Testes Ovaries & Pregnancy

  1. development of the reproductive system
    • hormones tigger development from sexually indifferent structures
    • fetuses start out with undifferentiated gonads (will become testes or ovaries) and undifferentiated internal structures
    • there are also undifferentiated external structures
  2. internal strucutures that embryos have
    • wolffian ducts: develop into male strucutres
    • mullarian ducts: develop into female
    • when sex is determined, the other duct will disintegrate
  3. undifferentiated external structures
    • labioscrotal folds
    • genital tubercle
    • these will develop into homologous structures in male and female
  4. what is key in sexual development?
    • whether there is a y chromosome or not
    • y chrom contains sex determining region on the SRY antigen
    • if no y, there is automatic female development
  5. development of male from embryo
    • start with embryonic gonad: if y chrom present the embryonic testis will develop
    • in the embryonic testis there is development of male internal and external structures and degredation of mullarian ducts
  6. degredation of mullarian ducts in male development
    sertoli cells of the embryonic testis produce mullarian inhibiting hormone which causes degredation of mullarian ducts
  7. development of male internal structures in male embryo development
    • interstitial (or leydig) cells of embryonic testis produce a small amount of testosterone
    • this testosterone will contribute to the development of the wolffian ducts into the male internal strucutes
  8. development of male external structures in male embryo development
    • interstitial cells of testis make a small amount of testosterone
    • while some of this T contributes to internal structure development, some is also converted to Dihydrotestosterone by 5alpha reductase
    • DHT then stimulates development of male external strucutres
  9. Disorders of development
    • klinefelter's syndrome
    • turners syndrome
    • androgen insensitivity
    • 5 alpha reductase deficiency
    • congenital adrenal hyperplasia
  10. Klinefelter's Syndrome
    • XXY chromosomes- person will develop as male, but will usually have a small testis and usually will be infertile- usually have small penis
    • people tend to be tall bc there is low T so less converted to E for bone calcification so more growth
    • some gynecomastia and some female body shape such as wider hips
  11. Turner's syndrome
    • person has 1 sex chromosome: X- so automatic female development
    • ovaries usually basic-therefore infertility common
    • women have uterus and vagina and can get preg through invitro fertilization tho
    • dont usually see secondary sex characteristics
    • people typically short
  12. Treatment of turner's syndrome
    oral contraceptives to develop reproductive structures and secondary sex characteristics
  13. androgen insensitivity
    • lack to testosterone receptor
    • a genetic condition- XY chromosmes but there is a mutation
    • high T bc testies in abdominal cavity and there is no negavtive feedback to shut off T production
    • have a blunt end vagina, breast development, female shape, T is converted to E by adrenal cortex
  14. treatment of androgen insensitivity
    removal of testes because they are not descended which is a risk for testicular cancer
  15. 5alpha reductase deficiency
    • genetic condition: for male external strucutres to develop in utero and secondary sex characteristics, you need conversion of T to DHT (which is more potent)
    • pateint is XY 
    • child may look female but may have sexually ambiguous genitalia (ie larger clitoris) but does go through puberty
    • at puberty- large increase in T and the person does develop external structures and some secondary sex characteristics (but not same hair changes that you normally see at puberty- no beard etc)
  16. congenital adrenal hyperplasia
    • genetic condition aka adrenal genital syndrome
    • person lacks the enzyme in the adrenal cortex to make hydorcortisone (not vital for life)
    • adrenal cortex keeps being stimulated by high levels of ACTH (no neg feedback) causing growth of cortex and the pathway to T gets amplified (more T)
    • person is XX- looks and has masculin characteristics but has female reproductive strucutres
    • there will be sexual ambiguity
    • if happens in a male there will be early puberty
  17. treatment of congenital adrenal hyperplasia
    hydrocortisone given causing neg feedback and a drop in Testosterone
  18. main androgen of male
    • testosterone
    • some made in adrenal cortex and ovaries in women
  19. precursors of testosterone
    • dihydroepiandrosterone
    • androstenedione
  20. how is testosterone released
    released in pulses but there is a daily rythem- its high in the morning and low later in the day
  21. How is tesosterone transported in the blood
    mostly bound to sex hormone binding globulin (a protein)
  22. Testosterone receptor
    • same receptor in the target cell for T and DHT
    • located in the nucleus of target cell
  23. metabolism of T
    when T is produced there is metabolism0 any excess gets broken down (primarily in the liver) and the metabolites of the T go into the bile and into the urine
  24. Functions of Testosterone
    • embryonic development of reproductive structures
    • stimulates spermatogenesis in the semineferous tubules of testes
    • stimulates sertoli cells in the semi tubes to make androgen binding hormone (with help of FSH)
    • stimulates the growth and development and functioning of the internal and external reproductive strucutres and influences the contents of the semen
    • vital for secondary sex characteristic development at puberty
    • stimulates bone growth and ossification 
    • causes body growth and increased muscle mass
    • stimulates kidney to make erythropoietin
    • affects behavior
    • negative feedback
  25. Testosterone in stimulating spermatogenesis in semi tubes
    • this happens from both T and FSH
    • when a boy is 11-13 interstitial cells start making more hormone, they undergo hypertrophy (growth) and hyperplasia (more of them) and become active making T
    • between 11 1/2 and 14 boys begin making mature sperm
  26. androgen binding hormone
    • binds to testosterone to keep it in the semitubes to enhance spermatogenesis
    • made in sertoli cells- stimulated by T and FSH
  27. How does T influence the semen
    • keeps semen rich in nutrients, esp fructose (energy source) and prostaglandins (from prostate gland) which can cause contraction of female organs to move sperm along
    • makes sure there is an alkaline pH of substance secreted to counteract acidity of male urine and woman's vagina
  28. How is T vital for secondary sex characteristic development at puberty?
    • pubic and axillary hair- male pattern hair on head, face, body
    • causes secretion of oil from sebaceous glands, thickening of skin, enlarged larynx and voice changes
  29. T in stimulating bone growth
    • stimulates bone growth and ossification (hardening) including deposition of calcium
    • some of this is directly from T while some is from T that has been converted to E
  30. T in causing body growth and increasing muscle mass
    • T is a protein and anabolic steroid- which causes body growth and causes increase in muscle mass and other soft tissues (liver, kidney, etc)
    • there is no coupling with/conversion to E in this
    • growth of reproductive structures will occur first
  31. Erythropoietin
    • hormone made from the kidney- synthesis stimulated by testosterone
    • stimulates blood cell synthesis (esp RBCs) in bone marrow
  32. Testosterone effect on behavior
    affects brain by stimulating libido and some aggression or competitiveness
  33. T in negative feeback
    • neg feeback on hyp and anterior pit
    • the body maintains homeostasis of T in the blood and sperm production
  34. Abuse of anabolic steroids (T or T- like hormones)
    • purpose is to increase muscle mass, but the level will cause neg feedback on the system causing decreased sperm count and decreased growth of reproduction organs
    • decreases FSH and LH in your own body which will decrease your natural T
  35. Side effects of anabolic steroid abuse
    • roid rage- effects brain for behavioral changes
    • acne
    • gynocomastia- from extra T converted to E
    • short stature in teens (t-->e causes closure of epiphysis/ bone calcification)
    • a lot of T usage is in liver- very vulnerable to damage and cancer
  36. aging in men
    • no menopause in men 
    • in manopausal woman- E plummets and no egg production
    • in men aging, there is a decreased sensitivity of gonads to LH then a decrease in T- but slower and more gradual than the decrease of E at menopause
    • decreased sperm production but still sperm and still fertile where women stop ovulation
  37. Sexual activity in men (before stimulation)
    before man is aroused and is resting- the symp NS is inhibiting the smooth muscle of the arteries of the penis- keeping it flaccid
  38. sexual activity of men- at stimulation
    • on stimulation, nitric oxide is stimulated by parasymp NS causing dilation of penis blood vessels and it engorges with blood causing an erection
    • nitric oxide acts through the cyclic messenger GMP
  39. Viagra
    viagra works bc it blocks cyclic GMP degredation, which gives more Nitric oxide, allowing erection to last longer
  40. Ejaculation
    sympathetic NS will cause contraction of smooth muscle of reproductive organs
  41. Regulation of testes through hormones
    • hypothalamus makes gonadotrophin releasing hormone which travels via portal blood to the gonadotrophs of the ant. pituitary 
    • when this happens the ant. pit is stimulated to make LH and GRH along with activins stimulate FSH production- both are released into the bloodstream
    • LH affects the interstitial cells of the testes to produce testosterone 
    • FSH stimulates the sertoli cells of the semi tubes to make androgen binding protein and inhibin for feedback; also stimulates spermatogenesis in semi tubes
  42. feedback in testes
    • when T is high it has a direct effect on the ant pit to shut off FSH and LH and on the hypothalamus (more important) to shut off GRH
    • FSH stimulates sertoli cells to make inhibin so when sperm is high  it will have direct effect on ant pit by blocking activins which stimulate FSH production and also it will inhibit hyp from producing GRH
  43. What kind of molecules are activins and inhibin?
  44. activins
    • made by gonadotrophs of the ant pit and the germ + sertoli cells of the testes 
    • help to stimulate FSH production
  45. ovaries
    • as gonads they make the sex cells or ova
    • make hormones-mostly steroids
  46. forms of female sex cells
    • form released at ovulation: oocyte
    • mature form formed by the completion of meiosis only happens when there is fertilization
  47. most important steorids made by ovaries
    the estrogens and progestins
  48. main estrogen
    • E2- 17 beta estradiol- gets converted to estrone which gets converted to estriol (in pregnancy, in liver and placenta)
    • estradiol is most potent estrogen
    • E2 is the main product of the follicle cells in the ovary and there is some progesterone
  49. main progestin
    • progesterone
    • progesterone is the main product of the corpus luteum, but there is also significant estrogen
  50. how are e and p transported in the blood
    both are bound to plasma proteins, just like tesotsterone and are inactivated by the liver
  51. Hormones from the ovary
    • mostly steroids
    • others include- peptides, glycoproteins, inhibins, relaxin
  52. peptides or glycoproteins made by the ovaries are called
    • intrafollicular regulatory proteins
    • they are important for oocyte maturation (ex- oocyte maturation factor, ovarian growth factor, activins, follistatin)
  53. inhibin hormones made by ovaries
    inhibings A+B- important in the menstrual cycle
  54. relaxin
    • important in pregnancy
    • comes from corpus luteum and placenta
  55. menstrual cycle rythm
    • a monthly rythem
    • even thought the body maintains homeostasis of ovary hormones, there is a rythem where levels change
    • rhythm is appx 28 days
    • rythm starts at menarchy (first period) and ends at menopause when the cycles stop
    • when we count cycle- start counting on 1st day of menses
  56. in the menstrual cycle, when do ovulation and menses happen
    • ovulation occurs appx 14 days after first day of menses
    • if no pregnancy, then menses will start appx 14 days after ovulation
  57. menses
    there is expulsion of superficial layers of endometrium lining the uterus and contraction of the myometrium of the uterus (contraction caused by prostaglandins)
  58. menstrual cramps
    • called dysmennorhea 
    • cased by contraction of the uterus which is caused by prostaglandins
  59. 2 main parts of menstrual cycle
    • events in the ovary (ovvarian cycle)
    • events in the uterus (endometrial cycle)
  60. hormone production in the ovary
    • follicle functions in hormone production before ovulation
    • corpus luteum functions after ovulation
  61. hormone production by follicle cells before ovulation
    • thecal cells produce androgens-androstenedione and testosterone
    • androstenedione and t then diffuse into granulosa cells
    • the granulosa cells have FSH present in them and when FSH enters them it stimulates aromatase, which stilmulates estrogen synthesis in the granulosa cells
    • FSH also stimulates granulosa cells to synthesize LH receptors, so follicle will respond to both FSH and Lh
    • granulosa cells also then make inhibin B-in early follicular phasae estrogen and inhibin B together cause negative feedback on FSH, resulting in selection of the follicle with the most FSH responsive cells to develop
  62. aromatase
    • stimulated by FSH when it binds to receptors in granulosa cells
    • stimulates estrogen synthesis in granulosa cells by..
    • --converting androstenedione to estrone (weak)
    • --converting testosterone to estradiol
  63. inhibin b (involvement in follicular phase hormone production)
    in early follicular phasae estrogen and inhibin B together cause negative feedback on FSH, resulting in selection of the follicle with the most FSH responsive cells to develop
  64. Day before ovulation
    • there is a surge (release in big spurt) in LH which stimulates
    • --small amount of progesterone (made by granulosa cells) from follicle before ovulation
    • --ovulation itself (stimulated by LH along with help of FSH, E and P)
    • --Lutenization after ovulation- formation of corpus luteum from follicle cells- follicle cells involute forming CL
    • --production of large amount of P and significant E after ovulation
  65. Corpus Luteum- functions in hormone production after ovulation
    • LH stimulates differentiation of granulosa cells to corpus luteum cells (formation aided by angiogenic factors made by granulosa cells, which also increase blood supply to CL)
    • CL produces inhibin A, which inhibits FSH by causing neg feedback
    • regression of CL due to prostaglandin from CL cells and uterus - form scar, corpus albicans forms from CL
    • as LH decreases, CL degenerates and progesterone and estrogen decrease
    • physical degeneration of CL due to prostaglandins
    • you need high E and P to keep endometrium of uterus thickened
  66. granulosa lutein cells
    mature CL cells
  67. how long is the cl maintained
    • about 14 days unless pregnancy
    • if pregnancy, human chorionic gonadotropin made from early placenta will mimic LH and keep it developed in pregnancy
  68. Feedback in menstrual cycle before ovulation
    • negative feedback by estrogen and inhibin b to select follicle that will mature
    • then E wil cause positive feedback on ant pit, stimulating a surge in FSH and LH right before ovulation
  69. Feedback in menstrual cycle after ovulation
    after the egg is released, corp lue is making E and P which will get high and have negative feedback on the hypothalamus and ant pit
  70. Gonadotropin releasing hormone release from hyp
    • released in pulses
    • stimulates both gonadotropins
    • slow frequency stimulates FSH high frequency stimulates LH
  71. overall production and regulation of gonadotropins
    • hypothalamus makes and secretes GTRH which travels via portal blood to ant pit and stimulates release of FSH and LH which both stimulate the ovaries for ovulation
    • FSH stimulates follicle cells of ovaries to make E and a little p
    • LH stimulates P and less E from CL
    • high P and E from CL cause neg feedback on ant pit and hyp
    • E and inhibin B cause neg feedback on hyp and ant pit to select follicle that will mature
    • E will cause pos feedback for surge of LH and FSH to cause ovulation
  72. menstrual cycle again step by step
    • 1. corpus luteum dies, e and p levels fall, bc there was only that 1 peak in LH
    • 2. pituidary responds to low e and p (no neg feedback) by increasing FSH secretion
    • 3. FSH recruits a cohort of large antral follicles to enter rapid growth phase, follicles secrete low amounts of E and inhibin
    • 4. E and inhibin negatively feedback on FSH
    • 5. Declining FSH levels cause degredation of all but 1 follicle- leading to selection of dominant follicle, which will produce high levels of E (estrogen peak before FSH and LH peak)
    • 6. High E has positive feedback on gonadotropes- LH and some FSH surges
    • 7. LH surge causes metabolic maturation, ovulation and lutenization; CL productes high P and significant E and inhibin A
    • 8. high P, E and inhibin A cause neg feedback making FSH and LH return to basal levels
    • 9. CL progressively becomes less sensitive to basal LH- dies if levels of LH like activity dont increase
  73. E + P in birth control
    prevent usual peaks in FSH and LH and therefore ovulation
  74. menses
    Low E and P cannot support endometrium of uterus so it sloughs off causing menses
  75. Mechanism of action of E and P
    • there steroids and have receptors in the nucleus of the cell
    • they affect transcription
  76. Receptor types of estrogen
    • Estrogen Receptor alpha: generally stimulates transcription
    • Estrogen Receptor Beta: generally inhibits transcription
    • some target cells only have one type some have both, depends on nature of the tissue
  77. Functions of estrogen
    • Stimulates the ovaries
    • Functions in puberty
    • Stimulates growth and development and functioning of secondary sex structures
    • Stimulates Growth and maturation of bone
    • Has cardiovascular effects and benefits
    • Maintains smooth skin in women
    • Affects adipose Tissue
    • Affects brain
    • Affects digestive tract
    • Affects kidney
    • Feedback
  78. Estrogen stimulates the ovaries function
    • facilitates growth of the follicle (even though it is made by the follicle too- follicle is mostly stimulated by FSH but this is involved)
    • stimulates ovulation with LH, FSH, and progesterone
  79. Estrogen functions in puberty
    • increased production of it at puberty
    • girls start puberty appx 2 years earlier than boys (boys start 9-15, girls 7-13)
    • if children put on weight early on, an increase in weight can cause early puberty
    • leptin from adipose tissue has a permissive effect on hypothalamic function
    • adipose tissue can also make some steroids and if you have androgens they can be converted to estrogen so more fat can cause this contributing to early puberty
  80. Estrogen function in stimulating growth development and functioning of secondary sex structures
    • rythmic changes and changes in preg
    • E affects structures including fallopian tubes, uterus, vagina, breasts, and secondary sex characteristics of puberty
  81. E in growth/development/functioning of fallopian tubes
    e causes smooth muscle contraction and movement of the fibriae (fingerlike projections) to enhance chances of fertilization in fallopian tube
  82. E in growth/development/functioning of uterus
    • E causes thickened endometrium and the cervical secretions to be thin and watery before ovulation so the sperm can get through
    • at birth E causes contraction of the myometrium of uterus for birth
  83. E in growth/development/functioning of vagina
    E stimulates prolifferation (more of them) of cells and keratinization of the cell lining (for protection)
  84. E in growth/development/functioning of breasts
    the basic change it causes is in fat- causes increase of fat deposit and some (but not much) duct development (there will be much more duct development at pregnancy)
  85. E in growth/development/functioning of secondary sex characteristics of puberty
    • e causes some body configuration changes, overall increase in subcutaneous fat, wider hips
    • pubic and axillary hair due to E and androgens from adrenal gland
  86. Estrogen function in stimulation of growth and bone maturation
    • Estrogens stimulation of growth is in conjunction with growth hormone and insulin like growth factor
    • estrogen has a stronger effect on the ossification of bone than T does (so girls reach adult height earlier)
    • E stimulates osteoblasts (bone forming cells) in number and funcitoning
    • E stimulates Ca2+ deposit in bone
    • E inhibits osteoclasts (bone destroying cells)- at menopause significant drop in Ed so women more at risk for osteoperosis bc bone more vulnerable
  87. Estrogen function in cardiovascular effects and benefits
    • until menopause, women have less risk for heart attack and stroke compared to men (after menopause equal risk)
    • E has a positive effect on cholesterol (made in liver)- decreases blood cholesterol level
    • E stimulates vasodilation (widening of blood vessels)
    • E decreases platelet activation slowing blood clot formation in healthy bvs
    • overall E increases blood flow
  88. how specifically does E help blood cholesterol levels
    • lowers blood cholesterol level
    • decreases LDL (which keeps cholesterol in the blood) and increases HDL (which gets cholesterol out of blood)
  89. how exactly does E stimulate vasodilation (widening of blood vessels)
    stimulates vasodilation by stimulating nitric oxide which will give more room for blood to move through to reduce risk of blood clots
  90. How does E maintain smooth skin in women?
    • does this along with P 
    • both stimulate collagen (important in connective tissue elements of skin) synthesis
    • E stimulates proliferation of skin cells, promoting wound healing
  91. Estrogen effect on adipose tissue
    • E decreases adipose tissue development in other parts of the body, besides breasts
    • at menopause there is increased deposit in adipose tissue (esp in abdomen), there is also decreased metabolic rate from time but mostly bc of low E
  92. Estrogen affect on the brain
    • influences behavior, including libido (with help of adrenal androgens)
    • E has positive effect on some protection of neural cells from degredation
    • E has some effect on communication ind cognition
  93. Estrogen effect on digestive tract
    helps stimulate calcium absorption
  94. Estrogen effect on Kidney
    E helps decrease blood pressure by decreaseing blood volume by increasing sodium and water excretion
  95. Progesterone
    • effcts try to enhance and maintain pregnancy
    • Dominates over E after ovulation
    • increases in puberty and regnancy
  96. Gestation
    the length of pregnancy
  97. Where does Progesterine function?
    • ovaries
    • breasts
    • uterus
    • kidney
    • brain
    • negative feedback only (no pos) on hyp and ant. pit
  98. Progeterone in the ovaries
    • stimulates the release of oocyte at ovulation
    • stimulates collagenase- breaks down collagen and frees up the oocyte
  99. Progesterone in the breasts
    • stimulates gland cell (cells that produce milk) development in pregnancy
    • complemantary to E's effect on breast development
    • womens breasts may feel lumpy after ovulation bc P causes fluid deposit in breasts when levels increase after ovulation
  100. Progesterone in the uterus
    • complementary to E's effect on uterus
    • maximizes the blood and nutrients in the fully developed endometrium after ovulation
    • makes endometrium ready for implantation
    • thickens cervical secretions for protection incase there is a pregnancy after ovulation
    • inhibits contraction of myometrium and dominates over E to prevent miscarriage in preg-important for keeping embryo implanted
  101. Progesterone in the Kidney
    like E, decreases blood volume and pressure by increasing water and sodium excretion
  102. Progesterone in the Brain
    • increase in P after ovulation causes a slight increase in metabolic rate which will increase during pregnancy- effects hypothalamic temperature center
    • P affects respiratory centers in brain stem to make them more sensitive to CO2 to regulate breathing
  103. Menopause
    • It is climacteric- the gradual decline in ovarian function
    • theres a decreased response of the ovaries to FSH and LH
    • there will be no ovulation and a decrease in estrogen and progesterone- this causes high FSH and LH bc low P and E so no neg feedbac
  104. When is menopause complete
    you can have years of irregular cycles, but menopause is complete after one year of no menses
  105. Effects of decreased estrogen in menopause
    • increases risk of osteoperosis
    • increases vaginal dryness/thinning
    • decreases elasticity and thickness of skin
    • increases risk of cardiovascular disease (heart attack and stroke) to equal mens risk
    • cuases vasomotor disturbances (temporary and variable)- hot flashes and nightsweats- caused by changes at hypothalamic level
  106. How to decrease risks associated with low E in menopause
    • Change diet
    • medications 
    • hormone replacement therapy
  107. change in diet to decrease risks associated with low E in menopause
    a diet with adequate calcium and vitamin D and exercise can decrease risk
  108. How do osteoperosis medications work in to decreasing risks associated with low E in menopause
    they decrease the number and activity of osteoclasts (bone destroying)
  109. Hormone Replacement Therapy to decrease risks associated with low E in menopause
    • giving estrogen- not reccomended for women over 50 bc it increases the risk of heart attack and stroke and increases risk of breast and endometrial cancer as well as ovarian cancer
    • in aging, E's effect on cholesterol is wiped away which causes these problems
  110. Other possible medications to decrease risks associated with low E in menopause
    • Tomoxifan
    • Raloxifene
  111. Tomoxifan
    • used to decrease risk of breast cancer, it is an antagonist to estrogen (blocks receptors) in breast cancer but is agonistic (stimulatory, has positive effect) on bone
    • can increase risk of endometrial cancer
  112. Raloxifene
    • an agonist to E for bone but an antagonist to the breast and uterus
    • still under study
  113. Disorders of ovaries
    • ovarian cancer
    • polycystic ovarian syndrome
  114. ovarian cancer
    • has no obvious early signs
    • usually diagnosed late after it has already spread
    • symptoms: abdominal bloating, urge to urinate
    • decreased ovulation decreases risk: oral contraceptives, young 1st pregnancy, breast feeding)- women who have never been preg have higher risk
  115. Polycystic ovarian syndrome
    • 12+ cysts (fluid filled growths) in an ovary
    • contributes to 10% of infertility in women
    • associated with obesity and insulin resistance
    • you dont have the usual pattern of FSH and LH secretion- so you dont have a dominant follicle that develops and therefore no normal ovulation
    • a # of follicles develop and then stop- creating cysts
    • there is increased secretion of androgens- decreased conversion to E2 but increased estrogen causing hirsuitism (abnormal hair growth) and acne
  116. Polycystic ovarian syndrome treatments
    • weight loss
    • clomaphine 
    • surgery to remove cysts
    • if a person doesnt want to be pregnant, oral contraceptives can be given- has positive E effects and decreased T effects
  117. clomaphine
    (fertility drug)- an estrogen receptor agonist- blocks E receptor preventing neg feedback allowing an increase in FSH and LH which can trigger normal ovulation
  118. what factors increase T in male and increase E and P in female? in puberty
    • first increase gonadotropin releasing hormone from hypothalamus which will influence pituitary and then gonads
    • body weight and leptin (hormone in fat)
    • decreased melatonin
    • kiss1 gene
  119. melatonin in puberty
    • supresses reproduction by affecting hormones
    • when people are children they have high melatonin and sleep alot- level decreases as you age and when this happens it may have a permissive effect on reproductive hormones
    • levels are higher in dark and lower in light- girls who are blind have later puberty
  120. Kiss1 gene
    • codes for a polypeptided called kisspeptin
    • has receptors in hyp + adrenal cortex
    • puberty associated with increased kiss1gene expression which acts like increased Gonadotropin releasing hormone
  121. Infertility
    • the inability to acheive a pregnancy after 1 year of unprotected intercourse
    • usually theres a minimum of 6months before any treatment
    • ~15% of couples trying to have kids have this
    • of these couples 40% male fault 40% female fault 20% both fault
  122. What are many fertility drugs used for
    • to treat anovulatory disorders (lack of ovulation)
    • or to stimulate ovulation for the retreval of eggs for invitro fert. or other assisted reproductive technologies
  123. superovulation by drugs
    drugs and hormones that cuase the body to make its own FSH and LH are less likely to cause superovulation compared to drugs/hormones that directly stimulate ovulation
  124. Fertility drug list
    • Clomid (clomiphene citrate pill)
    • Parlodel (bromocriptine) pill
    • FSH (Metrodin)
    • HMG (Pergonal)
    • HCG (Pregnyl)
    • GnRH (Factrel)
    • Lupron
    • Antagon
  125. Clomid (clomiphene citrate) pill
    • first go to drug if woman not ovulating but has healthy fallopian tubes (doesnt need IVF)
    • Binds to E receptor and blocks neg feedback of E on hyp and pit- causes woman's body to make GnRH, LH, and FSH (her own) which stimulate ovulation
    • shes more likely to have only 1 kid bc causes her to make her own LH and FSH so no superovulate
  126. Parlodel (bromocriptine) pill
    • used when abnormally high prolactin inhibits ovulation (natural effect of prolactin)
    • drug inhibits prolactin and ovulation occurs normally
  127. FSH (Metrodin)
    • used to be isolated from postmenopausal woman's urine
    • now FSH synthesized by recombinant DNA technology
    • this is an option if clomid doesnt work
    • FSH directly stimulates ovulation
    • this method can cause multiple eggs to develop
  128. HMG (Pergonal)
    • another option if clomid doesnt work
    • human manopausal gonadotropin, isolated from postmenopausal women
    • contains both FSH and LH which stimulate ovulation
  129. HCG (Pregnyl)
    • isolated from preg. womans urine or HCG synthesized by recombinant DNA technology
    • Human chorionic gonadotropin- acts like LH and stimulates ovulation
    • often used in conjuction with other fertility drugs (FSH or HMG) but can be given alone
  130. GnRH (Factrel)
    • synthesized by recombinant DNA technology
    • gonadotropin releasing hormone stimulates woman to make her own FSH and LH, stimulating ovulation (no overovulation bc she makes her own)
    • rarely used in USA
  131. Lupron
    drug that is GnRH agonist- acts like GnRH to stimulate woman's production of her own FSH and LH, which stimulate ovulation
  132. Antagon
    • Drug that is a GnRH antagonist- suppresses FSH and LH 
    • specifically used to prevent premature release of eggs for invitro fert. so eggs can be retreived from ovary.
  133. Types of Contraception- birth control
    • Understanding of hormones
    • breast feeding
    • combined estrogen and progesterone
    • progesterone only methods
  134. Understanding of hormones- birth control
    • no intercourse when fertile- no artificial birth control
    • 1. pinpoint day of ovulation and/or signs after ovulation
    • 2. five days before ovulation- as sperm can remain viable up to 5 days
    • 3. 1 day after ovulation, egg is viable for 24 hours
    • this is most reliable only if woman has a regular cycle
  135. examples of pinpointing day of ovulation or looking for signs after
    • pinpointing day: ovulation predictor kits measure LH surge in urine one day before ovulation
    • signs after ovulation: slight increase in basal body temp and thickened cervical mucous
  136. Breast feeding as birth control
    • natural birth control- as prolactin inhibits hormones of the cycle and therefore ovulation
    • has led to natural spacing of children, but note ovulation occurs 2 weeks before menses
    • Time varies, and not totally reliable esp when some feedings are replaced by solid food
  137. Combined estrogen and progesterone methods birth control
    • take hormones for 3 weeks then no hormone for 1 week
    • by neg feedback, E and P inhibit hypothalamus and pituitary- prevents usual patter of FSH and especially LH and therefore prevents ovulation
    • types: the pill (oral contraceptive); other methods (patch, vaginal ring)
  138. Why does menses occur on combined E and P pill?
    • menses occurs bc endometrium builds up with hormones and then sloughs when no hormones
    • menses occurs but ovulation doesnt
  139. progesterone only methods- birth control
    • works primarily by preventing fertilization, may or may not prevent ovulation
    • types: mini pill; other methods such as implanon and depo-provera shot
  140. mini pill (progeterone only pill)
    works primarily by thickening cervical mucous, altering endometrium and decreasing fallopian tube motility
  141. implanon
    implanted capsule under skin (works up to 3 years unless removed)
  142. Depo-provera shot
    works for 3 months
  143. Emergency contraception
    • not a regular birth contraception
    • morning after pill
    • mifepristone
  144. Morning after pill
    • different types; high amount of oral contraceptives
    • some P only, some E and P
    • Plan B is an example
  145. Plan B
    • synthetic progestin only pill
    • can use up to 3 days after unprotected sex, but after 1 days (may be effective up to 5 days)
    • if a woman hasnt ovulated it can prevent ovulation, if she has it can prevent fertilization or implantation
    • implantation is about a week after fert. if implantation has occured it will not work
  146. Mifepristone
    • pill inducing menstration
    • can use for longer time than Plan B- up to 49 days
    • can use whether pregnant or not 
    • works as progesterone antagonist, thus, anti progesterone action
    • after pill 48 hrs later take prostaglandin (pill or vaginal insert) which contracts uterus and expels heavy (with tissues if pregnant)
  147. Placenta
    • an endocrine gland
    • forms partly from the mothers endometrium and partly from the outer fetal membrane (chorion)
    • fetal and maternal blood dont mix although things go back and forth between them
    • also called the fetal placental unit
  148. hormones of pregnancy
    • almost all produced by placenta
    • Human Choreonic Gonadotropin
    • Human Placental Lactogen
    • Human Growth Hormone Placental Varient
    • Parathyroid Hormone Related Protein
    • Relaxin
    • Estrogen
    • Progesterone
  149. Human Choreonic Gonadotropin (HCG)
    • Formed from the tiny beginning placenta
    • prescence of this int he urine is the basis for preg- can be detected in the blood 1 day after implantation 
    • as the placenta makes its own E and P, HCG decreases, but remains present
    • high sensitivity, we only need a little for an effect
  150. stimulation and mechanism of HCG
    • stimulates the gonads- acts like LH to prolong the life of the corpus luteum in the mother;s ovary
    • binds to LH receptors- its a glycoprotein very similar to LH- and keeps up E+P production in the ovary in the first 10 wks of preg
    • vital in first trimester bc it keeps endometrium developed indirectly and does not contract myometrium- critical for maintaining pregnancy
  151. Human placental lactogen
    • a protein that increases as HCG decreases (not a direct effect tho); increases in preg, affects mom and fetus
    • acts like growth hormone for the fetus
    • mobilizes nutrients in the mother's blood to go through the placenta to the fetus
    • shifts the moms metabolism to use more fat
    • stimulates mammary gland growth in breasts
  152. how does human placental lactogen act like growth hormone for the fetus?
    works via insulin like growth factor to stimulate fetal growth
  153. why does human placental lactogen shift the moms metabolism to use more fat?
    • the fetus concentrates glucose as a main energy source so fetus uses glucose mom uses fat
    • if this isnt successful, a small % of women develop guestational diabetes- will dissappear after birth-they will have incr. risk of type II diabetes later in life tho
  154. Human Placental Lactogen in stimulating mammary gland growth
    acts like prolactin and development of the breast involves a number of hormones including this one
  155. Human Growth Hormone Placental Varient (HGHPV)
    • A protein very similar in structure to growth hormone- helps in growth
    • helps mothers metabolism to promote protein synthesis
  156. Parathyroid Hormone Related Protein
    • parathyroid hormone normally increases blood Ca2+ when low
    • this increases the transport of Ca2+ from mothers blood to placenta to fetus
  157. Relaxin
    • a polypeptide that comes both from the mothers corpus luteum and placenta
    • highest in 1st trimester (when CL is most significant)
    • stimulates blood vessel development in the placenta
    • these above functions are mostly known in animals, not 100% sure for humans
  158. Relaxin before birth
    • relaxes pelvic ligaments and dilates cervix/vagina to facilitate birth
    • not sure of significance in humans but E+ P help in this
  159. Estrogen (hormone of pregnancy)
    keeps increasing and increasing during pregnancy (first from corp. lut then more from CL)
  160. Main type of estrogen in pregnancy
  161. Estriol funcitons in pregnancy
    • causes growth of uterus and vaginal tissue
    • enlarges external genetalia and widens vaginal opening
    • relaxes pelvic ligaments and pubic symphysis- allowing stretching for bith
    • changes many aspects of maternal physiology (bc her body needs to give nutrients and excrete both their wastes)
    • helps to induce elements important in birth
    • tends to stimulate uterine contractions
  162. Estriol functions in pregnancy breasts and lactation
    • increase in ducts and fat in breasts
    • increases prolactin which in turn increases breast development (but progesterone still inhibits milk production at this point
    • stimulates hydrocortisone (from adrenal cortex) which will facilitate lactation after birth
  163. aspects of maternal physiology changed by estriol in pregnancy
    • 50% increase in blood volume
    • increased efficiency of excretion by kidneys
    • these are bc she needs to have nutrients for both herself and fetus and excrete both their wastes
  164. Estriol effects on brain in pregnancy
    causes neg feedback on hyp releasing hormone and pituitary FSH and LH so no ovulation or menses in pregnancy
  165. elements in birth induced by estriol
    • prostaglandins in the uterus
    • induces oxytocin receptors in the uterus
  166. Estriol function in stimulating uterine contractions
    tends to stimulate uterine contractions however it is dominated by progesterone which inhibits the contraction until birth where there is a shift in P sensitivity so birth can start
  167. Progesterone in pregnancy (body)
    • increases the deposit of nutrients in the endometrium (where embryo implants)- carb, protein, fats
    • inhibits uterine contractions during pregnancy so it will sustain the implantation- does this directly and also inhibits prostaglandins in uterus which stimulate contractions
    • affects the mothers respiratory centers to make them more sensitive to gases for more efficient respiration
  168. why does progesterone affect the respiratory centers
    • for more efficient respiration
    • o2 needed to support an increase in metabolic rate in the mother so better breathing=more o2 for this
  169. Progesterone in Pregnancy (breasts)
    stimulates development of glandular cells of breasts and deposit nutrients in breasts (to make milk)inhibits milk synthesis even though it causes development
  170. Parturition (Birth)
    • involves neuroendocrine reflexes (along with lactation)
    • expulsion of the newborn
    • labor and delivery involves hormone interaction and neuroendocrine mechanism
  171. Order of birth
    • 1. Labor
    • 2. Change in relationship between E+P
    • 3. Fetal hypothalamus has increased ACTH releasing hormone
    • 4. Estrogen stimulates mild uterine contractions
    • 5. Prostaglandins stimulated by estrogen
    • 6. Uterus becomes more sensitive to oxytocin and contracts with more force
    • 7. Dilation of cervix
    • 8. Oxytocin in birth
    • *amnion can rupture and fluid come out at anytime
  172. Labor
    • you build up strong uterine contractions
    • once you start it, youll have increased sensitivity of muscle to horomones and stronger contraction
    • a muscle contracts with more force after it has already contracted
  173. Relationship between E and P changes
    • up to this point, both E and P are very high, P dominates
    • uterine receptors become less sensitive to P and Estrogen will dominate
    • there may (not always) be decreased in P towards end of pregnancy
  174. Fetal hypothalamus has an increase in ACTH releasing hormone
    • this will stimulate an increase in fetal ACTH which will in turn increase hydrocortisone production
    • this hydrocortisone stimulates the placenta in the mother to make more estrogen
  175. Estrogen stimulates mild uterine contractions
    • estrogen will start uterine contractions- stimulates mild, rhythemic contractions (10 mins apart then 5 mins apart, etc)
    • these contractions from E are like menstraul cramps, not strong enough for birth
  176. Estrogen stimulates prostaglandin production
    • prostaglandin production is in uterus (which is now less sensitive to P)
    • prostaglandins then stimulate uterine contractions
    • prostaglandins inhibit and decrease the amount of P and increases oxytocin secretion (while E is increasing oxytocin receptors in uterus)
  177. Uterus becomes more sensitive to oxytocin and contracts with more force
    • the mechanical contraction and dilation (widening + shortning) of cervix increases the force of contraction and will send nervous impulses to hyp
    • when hyp gets this nervous impulse it will increase oxytocin synthesis which goes via neuron to post pit then to blood
    • neuroendocrine reflex- nervous stimulus hormonal response
  178. Dilation of the cervix
    due to estrogen, prostaglandins and possibly relaxin
  179. Oxytocin in birth
    • causes stronger tetanic (sustained) contraction of uterine muscle
    • abdominal contraction (mother pushing) aids in expulsion of the fetus
    • typical delivery is vaginal where head comes out first
  180. Afterbirth
    • uterine contractions expell afterbirth 
    • it is the placenta and fetal membrane
  181. Lactation
    breast development and milk production
  182. Breast development hormones
    • involves many hormones: E, P, Prolactin, Human placental lactogen (main reproductive hormones)
    • there are some non reproductive hormones that facilitate breast development and the ability to lactate: thyroid hormone, hydrocortisone, growth hormone, insulin
  183. Milk production + secretion
    • when the placenta leaves the body at birth, there is a decrease in E + P; this will allow prolactin to stimulate milk synthesis
    • a neuroendocrine reflex
  184. Neuroendocrine relfex of prolactin secretion in lactation
    • the nursing of a baby on breast causes sensory impulses to travel to the hypothalamus which will turn off the inhibiting hormone (dopamine) and therefore stimulate the anterior pituitary to make prolactin
    • prolactin then stimulates milk synthesis from nutrients in the glandular cells of the mammary glands of the breast
    • it also helps to maintain breast development and inhibit gonadotropic hormones- no ovulation/menses (can come back at anytime)
  185. Milk Release/ Letdown
    • neuroendocrine refles
    • the nursing on breast sends sensory impulses to hyp which makes oxytocin which goes to post pit then into blood causing contraction of myoepithelial cells surrounding the glandular alveolar cells in the breast
    • the milk will be pushed into the ducts (appx 15 of them) and out nipple
  186. 1st milk
    • collostrum
    • very rich in antibodies
    • mature milk takes about a week to develop
  187. Methods of treating infertility
    • enhance chances of fertilization
    • fertility drugs
    • surgery
    • insemination
    • insemination by donor
    • intrauterine insemination
    • invitro fertilization
    • IVF with donated egg or embryo
    • intracytoplasmic sperm injection
    • gamete intrafallopian transfer
    • zygote intrafallopian transfer
    • surrogacy
  188. Enhance chance of fertilization when there is no specific cause of infertility
    • timing sexual intercourse for ovulation
    • ID time by signs and ovulation predictor kit- measures LH peak 24 hours before ovulation
  189. enhance chances of fertilization when there is a problem with the male
    • high body temp can decrease sperm count and motility and tight clothes keep testes close to body
    • loose clothes can keep them cooler
    • avoid drugs, alcohol and smoking
  190. enhance chances of fertilization in overweight or underweight women (they have decreased fertility)
    • acheive normal body withg
    • leptin hormone in fat tissue stimulates GnRH in hypothalamus and ovulation
  191. When to use fertility drugs
    • woman is not ovulating
    • hormonal problem
    • men- possible hormone problem that affects sperm
    • medication will stimulate ovulation
  192. Surgery or drug
    • physical issue in men or women
    • correct a specific defect: varicocelectomy (twisted testicular blood vessels) in men or balloon tuboplasty (balloon inserted to open narrow fallopian tubes when blocked)
    • surgery or drug for endometriosis (extra endometrial tissue may cover the ovary or fallopian tubes)
  193. Insemination
    • used to treat low sperm count in someone that you want to be the biological father
    • semen with sperm are collected and samples are pooled
    • semen are directly introduced into the vagina or cervix
    • fertilization occurs in the women, frozen semen can be used
  194. Insemination by donor
    • Used for low sperm count, defective sperm, or no male partner
    • use of donated semen from sperm bank
  195. Intrauterine insemination
    • can be used for possible problem in man or woman
    • semen is introduced higher up (not in the vagina or cervix) in the body of the uterus increasing chances of fertilization
    • fertility drug may be given in addition to stimulate ovulation
  196. In vitro fertilization
    • developed for fertilization if woman has blocked fallopian tubes, but also for a variety of problems
    • fertilization outside of woman
    • semen is collected ova are removed from ovary after she has received fertility drug to cause superovulation
    • ovum placed in petri dish with sperm- fertilization occurs
    • Embryo (2-8 cells) transfered into uterus where embryo implants
  197. problems with invitro fertilization
    • hardest part is implantation of the embryo- only about a 30% success rate
    • more than one embryo may be implanted- twins
  198. IVF with donated egg or embryo
    • used when the woman cannot ovulate
    • donor of egg may receive fertility drug
    • hormone treatment of recipient for implantation
  199. Intracytoplasmic sperm injection
    • high tech way of resolving low sperm count, woman's allergy to sperm, or problem in woman
    • get the egg out of moms body and thin needle is used to insert single sperm into egg, fertilization occurs and early embryo implanted (30% success rate)
  200. Gamete intrafallopian transfer
    • used when fallopian tubes function, but there is low sperm count or other problem
    • ovum and sperm placed at the end of fallopian tube together and fertilization occurs there
  201. Zygote intrafallopian transfer
    • a variant of GIFT
    • fallopian tubes function, but low sperm count or other problem
    • like IVF- ovum and sperm combined in petri dish, but you put the zygote in the fallopian tube and it travels to the uterus on its own
  202. Surrogacy
    • used when woman cannot carry the embryo in her uterus (2nd tri miscarriage can indicate uterine problem)
    • if surrogate mother is inseminated with semen, she is biological mom
  203. gestational surrogate
    • surrogate is not genetic mother
    • either use ovum from wife and IVF or use donated embryo
Card Set
Testes Ovaries & Pregnancy
Exam of 10/16/2015