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Physiology II > Reproductive > Flashcards

Reproductive Flashcards

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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
Androgen receptors
Bind to aromatized androgens to promote growth an development of gonads and secondary sex characteristics Leydig cells will aromatize androgens (making testosterone, estrogens, DHT)
26
Three most active androgens in men
testosterone Dihydrotestosterone: higher affinity for androgen receptor. Synthesized from testosterone in some target tissues. Androstenedione: precursor of testosterone; 1/10 the activity
27
Transport of androgens
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
28
Active testosterone
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.
29
Excretion of testosterone
Converted to other metabolites. Converted in liver to DHEA and excreted through liver via bile or kidney via urine.
30
Testosterone secretion
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
31
Mechanism of testosterone
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
32
Converting testosterone
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)
33
Effect of taking end production androgens
It effectively works as a form of birth control. As GnRH is highly sensitive to the inhibitory effects of estradiol and testosterone
34
During puberty receptors
become desensitized due to increased concentration of testosterone and estradiol.
35
Regular circhoral expression of GnRH is established
At the end of puberty Sustains a regular secretion of gonadotropins sustains regular gonad production of sex hormone Establishes adulthood
36
Stimulation of Kisspeptin neurons
can be stimulated by either testosterone or estradiol | Kiss peptin stimulation will stimulate the development of GnRH
37
Lack of kisspeptin/receptor
Kallman's sydrome | Delayed onset of puberty
38
With increased testosterone in relation to FSH receptor
Greater Testosterone leads to more sertoli cells. Increases the metabolic capacity of sertoli. Greater density of FSH receptor and greater gametogenesis.
39
Testosterone in-utero
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"
40
Testosterone in puberty
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
41
Reproductive function of testosterone
Promotes secretion of male genital tract Required for normal sex drive Testosterone is essential for sperm maturation and semen production
42
Release of hormones in females
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.
43
HPG activity pre-puberty
HPG axis is very low or inactive until puberty when pulsatile secretion of GnRH establishes gonadotropin and ovarian hormone levels sufficient to stimulate menarche
44
Progestrin/estrogen and follicular phase and luteal phase
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
45
During the female reproductive phase progesterone and estrogen regulate changes in
``` Ovary Endometrium Secretion of GnRH Secretion of LH Secretion of FSH ```
46
GnRH feedback loops in females
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
47
Becoming a woman begins as a fetus
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
48
Eggs in the ovary with age
Gestation: 7 million Birth: 2 million Puberty: 400,000 Only 400 ova released at ovulation during reproductive ages.
49
Process to progress to an antrum
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
50
LH spike
Midcycle and stimulates ovulation Stimulates a change in the cells of the ovary to produce more lutenizing cells This defines the luteal phase
51
Menstrual cycle phases
Follicular phase first | Luteal phase second
52
What hormone builds with follicular phase
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
Follicular phase begins with...
Menses Uterine wall sloughs off Sex hormones are very low Gonadotropin levels are high
54
Follicular phase endometrial lining will rebuild with...
Increased estradiol levels Lining will reach a peak as one enters the luteal phase
55
Uterine Milk
Produced with high levels of pregesterone during the luteal phase Aids with implantation
56
Negative feedback to positive feedback switch is accomplished by
Reaching peak levels of estradiol at the end of follicular stage.
57
Granulosa cells
Surround the primary oocyte (ovum) to form primordial follicle Protect ovum
58
Primordial follicle cells are maintained throughout live by...
Oocyte maturation inhibitor produced by granulosa cells. Does so by preventing FSH receptor expression
59
As oocyte maturation inhibitor declines...
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
Each cycle six primordial follicles express enough _____ to become _____
FSH receptor preantrum follicle Process takes 300 days
61
Preantral (primary follicle) cell
Has a thicker layer of granulosa cells than primordial Progresses to antrum cells
62
Antrum (secondary follicle) is characterized by ___
Presence of thecal cells
63
Thecal cells
Once proliferation of granulosa cells by FSH receptor reaches a critical point thecal cells appear Express the LH receptor
64
The antrum
can produce sex hormones thanks to the thecal cells that differentiate at this stage. Thecal cells express LH receptor
65
Thecal cell hormone production
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
Antrum (secondary follicle) forms __ days before ovulation
65
67
During follicular phase thecal cells of antrum dominantly make ___
Estradiol May also make low levels of progesterone and testosterone
68
Inner granulosa cells of the antrum...
express FSH receptor and convert theca derived androsterone and tesosterone to estradiol FSH receptor signaling increases aromatase to produce estradiol
69
Estradiol production of females every month comes from
30-60 immature follicles with thecal cells
70
Selection of dominant pre-ovulatory follicles....
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
Thecal cells of the dominant preovulatory follicle
Can also produce estradiol
72
Dominant (graffian) follicle regulates GnRH, FSH, and LH
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
Inhibin in females is made by the...
dominant follicle around day 10 and will decrease FSH
74
Hypothesis about GnRH and LH surge
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
Tertiary follicle
Similar to the secondary follicle | Has antral fluid. Accumulates between the oocyte and granulosa layer and has FSH receptor tht can concentrate FSH
76
Dominant (graffian follicle)
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
Ovulation occurs...
14 days after teh first day of menses | 2 days before ovulation LH secretion drastically increazses
78
Sweling of the dominant follicle is caused by
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
Peak LH
converts granulosa cells and thecal cells to progesterone producing leutin cells and beginning the luteal phase requires appropriate levels of estradiol
80
Signs and symptoms of ovulation
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
Leutin cells
Produce low levels of inhibin that prevent FSH | If FSH is present in the luteal phase another cycle will start! (prevents fertilization)
82
Luteal phase
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
Progesteroen in luteal phase
produced by leutin cells Pro-Gestation 12 days post ovulation functionality for implantation
84
If not pregnant
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
If pregnant then
Placenta hCG will feed the corpus luteum for the entire first trimester
86
Uterine cycle
Fluctuation of the endometrium that coincides with the ovarian cycle Influenced by estradiol and progesterone
87
Complete lack of estrogen and progesterone
Seen with Corpus albicans | Leads to the destruction of the uterine lining and vasospasm
88
Fibrinolysis
Produced during menses to prevent blood clotting
89
Clots during menstruation
Indicates a uterine pathology
90
Uterine cycle endometrium
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
Female puberty is activated by...
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
Estrogen in menopause
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
Inhibin in menopause
Runout of dominant follicle and luteal cells which wil result in a sharp increase in gonadotropin with FSH levels higher than LH
94
Hormones during follicular phase
Progesterone, androstenedione, and testosterone are synthesized first but are all converted to estradiol by aromatase
95
Hormones during luteal phase
There is less aromatase which leads to excessive amounts of progesterone
96
3 types of estrogens
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
Progestins
Progesterone 17-a-hydroxyprogesterone with the same effects of progesterone
98
Progesterone secretion timing
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
Transport of female sex hormone
Use liver-derived Sex Hormone Binding Protein | Loose binding and hormones is released to tissue after 30 minutes
100
Metabolism of Female Sex Hormones
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
Endocrien actions in females
Estradiol: generallly proliferation and differentiation and growth of genital tract Progesterone: a secretion hormone, prepare uterus for pregnancy and breast for lactation
102
Estrogen actions
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
General estrogen actions
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
Estrogen excess
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
Estrogen deficiency
``` Scant menses Small uterus Small breasts Midcycle spotting Infertility due to lack of ovulation ```
106
Progesterone actions
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
Progesterone Excess
``` Edema (due to secretion) Bloating Headache (Hypertension) Depression (associated with lack of sleep) Weight gain Tiredness Hypertension, varicose veins ```
108
Progesterone deficiency
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
Hormonal contraceptives
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
Contraceptives have 4 types
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
Placenta derived hormones
hCG (Human Chorionic Gonadotropin) Estrogens Progesterone hCS (Human Chorionic Somatomammotropin)
112
hCG
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
hCG secretion
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
hCS Pattern of secretion
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
hCS actions
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
Progesterone synthesis in pregnancy
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
Progesterone action during pregnancy
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
Estrogen synthesis in pregnancy
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
More Hormone actions in pregnancy
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
Changes in mom with pregnancy
``` 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
Preeclampsia
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
Possible causes of preeclampsia
Placental and adrenal hormones (aldosterone) Autoimmune Insufficient blood to placenta
123
Placenta action
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
Oxytocin in third trimester
Receptor expression increases and allows positive feedback between oxytocin and uterine contraction initiated by dilation of teh cervix and fetal pituitary
125
Lactation
Extrogen will inhibit the production of milk | Prolactin aids lactation

Physiology II (4 decks)

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