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282 Cards in this Set
- Front
- Back
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What causes y chromosome to be fore males |
It codes for protein H-Y antigen needed for testicular development |
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Amount of eggs made from immature ova |
One |
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Gonodal sex |
Presence of testies or ovarys |
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What dictates gonodal sex |
Presense of y chromosome |
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When H-Y antigen appears for meales |
Week 7-8 |
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What happens if no H-Y antigen is present by week 9 |
Become female and have oogenesis occur at day 77-84 |
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What H-Y antigen causes |
Seminiferous toubules. Leydig cells. Testosterone peaks |
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What is present in undifferentiated gonads |
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What is left for males in gonads |
Prostate. Seminal vesicles. Vas reverend. Tested. Epididymis |
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Epididymis |
Attach testes to vas reverend |
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What remains for females in gonads |
Cumbria. Overies. Fallopian tubes and uterus |
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Phenotypic sex |
Outward apperance. |
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What determines phenotypic sex |
Gonadal sex |
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When external genitalia differentiates at |
Week 10 |
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Parts of an undiferenciates genitalia |
Genital tubercle. Urethral fold. Genital swelling. Anal opening |
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What the genital toubercle develops onto |
Gland penis or clitoris |
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What the genital swelling turns into |
Scrotum or labia |
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Hormonaly how females develop |
The lack of trigger hormones |
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What testosterone causes for ginadal development in males |
Wolgfian ducts differentiate. Cause male external genitalia to develop |
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What mis causes for in males |
Regression if mulmrtian duct |
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What causes Internal genitalia |
Presense or lack I'd testorone |
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What causes external genitalia diferientation |
DHT (males)or lack of |
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Gender idenity and genetics |
Not coded in gens |
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What androgens in early embryo causes |
More male behavior |
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Where androgens effect males |
Aromatization (E2) |
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Where females are protected from androgens |
Alphafetoprotein |
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Turners syndrome |
XO. Gonodal dysgenesis |
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Superfemale |
XXX |
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YO genetics |
Is lethal |
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Klinefelter syndrome |
XXY. Have seminiferous tubule dysgenesis |
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Two types of hormonal sexual abnormalityes |
Female and male psudohermaphroditism |
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Female psudohermaphroditism |
Make genitsila in genetic female due to androgens week 8-13. Congenital adrenal hyperplasia |
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Male psudohermaphroditism |
Female genitalia in genetic male due to defect in androgen synthesis or action. Testicular demonizing syndrome |
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How psudohermaphrodia is found |
Delayed orvabsense of puberitey by 17 in females and 20 on males |
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Panhypopituitarism |
Endocrine dysfunction |
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Primary amenorrhea |
Endocrine dysfunction |
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Gonodal dysgenesis |
Endocrine / genetic dysfunction |
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True precocious puberty |
Gamrtogenesis and secondary sexual chacteristics |
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Psrudkprecocious puberty |
Early secondary sexual chacteristcs by exposure to androgens for males and estrogen by females but no gametogensis |
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Negative long loop feedback of testosterone and ordtradiol |
Inhibit anterior pituitary and hypothalamus |
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What hypothalamus releases to stimulate sex hormones |
Gn-RH |
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What the pituitary relapses to release sex hormones |
LH FSH |
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What starts sex hormone release |
Early gonadal autonomous. Unrestricted release of pituitary gonadotropins. Negative feedback steroid at term. Neonatal stimulation due to loss of maternal steroids |
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What starts puberty theorys |
Critical size hypothesis. Missing link (positive drive) hypothesis. Gonadostat hypothesis |
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Menopause |
Stop of menstration at 45-55 years. |
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What causes menopause |
Depleated follicles and less resposive to gonadotropins. Estrogen and progesterone reduced |
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Climqcteric |
Make reduction in androgens |
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What causes climscteric |
Reduced sensaticity to LH. Reduced testies size. Reduced testorsterone production and action |
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Amount of time sperm must mature for |
10 day |
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What vasdefferns store |
Nutrients |
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Role of epididymis |
Sperm transport. Maturation. Motility. Fertility |
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Role of seminal vessicles |
Seminal fluid |
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What's in seminal fluid |
Fructose and prostaglandin |
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Prostate |
Alkaline prostatic fluid. Rich in prostaglandin |
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Prostaglandin |
Is a base |
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Bulbo-urethral gland |
Pre ejaculatory lubrication fluid |
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Penis |
Erection. Ejqctualtion. Intromission |
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Way blood flows to the testies |
Counter current |
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Role of counter current blood flow |
Venous blood cools arterial blood as they flow past each other |
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Temp of testicles |
2 degrees less then body temp |
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Extra function of counter current blood flow of tested |
Testosterone can leave vein and enter arteries beciase it's needed for gsmetogrnesis |
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Where sperm are made |
In seminiferous tubules |
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Two cell types if testies |
Spermatogrnic cells and interstitial cells |
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Role of interstitial cells |
Make testosterone |
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Amount of mass that is semeriferous tubules of testies |
80-90% |
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How semiferous tubules are decided |
Into lobules |
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Volume of testies |
18-20ml |
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Amount of lobules per testis |
250 |
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Length of seminiferous tubules |
800 feet/ testis |
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Cells that line the walls of the tubules |
Sertoli cells |
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What fsh causes in sertoli cells |
Testosterone to estradiol |
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What LH causes on leydig cells of men |
Cholesterol to pregnenalone to testosterone |
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Where DHT is made |
Mostly in target tissuev |
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Ways testosterone acts |
On receptor to form protein. Turns to estrodiol then protein. To DHT to protein |
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How testerostorne causes gametogenisis |
Act on sertoli cells which signal germ cells which lack testorsterone receptors |
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Testicular feminizing syndrome |
Androgen resistance or 5 alpha reductase deficiency |
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Cryptorchidism |
Undecended testicles |
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Juveinle hypogonadism |
Sexual immaturity due to low LH and FSH |
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Post pubertal hypogonadism (simmonds disease) |
Loss of testosterone and secondary sexual chacteristics |
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Stages of sperm production |
Mitotoc proliferation. Meiosis. Packaging |
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Cells of mitotic proliferation |
Spermatogonium. Spermatogonia. Primary spetmocyte all with 46 chromosome |
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How spermatogina work |
One stays on wall other becomes sperom |
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Cell types of meiosis |
Secondary spermatocytes. Spermatids |
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Packaging cell types |
Spermatozoa |
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How spermatogenisis function |
Move closer to lumen with each divide |
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Seperqtion from primary spermatocytes and secondary |
A tight junction |
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What signals all dividison up to secondary |
Autonomous |
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What starts final mitosis |
Testosterone |
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What starts final stage |
FSH |
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What maintains final stage of spermatogenisis |
Testosterone |
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Area with higher concentration of testosterone |
Lumen over plasma |
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What triggers waves of spermatovensis |
Phagocytosis of spermatozoan cytoplasm by sertoli cells |
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Role of sertoli cells |
Maintain blood testis barrier. Nurismnrt of germ cells. Produce seminiferois fluid. Eat old cells and spermatozoan cytoplasm |
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What sertoli cells produce |
Androgen binding protein. Inhibin and estrogen. Mullerian regressing factor (MRF) |
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Parts of sperm |
. Cap acrosome and flagellum |
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What happens to cytoplasm of sperm |
Buds off during development |
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What is on end if the head of a sperm |
Acrosome |
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What makes up tail of sperm |
Microtubules |
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What's in the midpiece of a sperm |
Mitochondria |
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Amount if semen ejaculated |
1-5ml |
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Amount of sperm ejaculated |
100mil / ml |
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Amount of sperm ejqculated to to be infertile |
Less then 20 mil |
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What majority of seamen is |
Seamen plasma |
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What the seminal vesicles produce |
45-80% of semen. Viscous secretion. Fructose rich. PG rich |
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What viscous secretion does |
Adhesion within the vagina |
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What PG causes |
Increased smooth muscle contraction in females tract |
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Amount if semen made by prostate |
15-30% |
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Things that the prostate secretion has |
Alkaline. Protease rich. PG rich |
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What protease causes |
Liquification of ejaculate after ejaculation |
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Cowpers gland (bulbourethral) |
Mucuus for vaginal penitration |
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What causes sperm movement in males |
Fluid pressure from : production from sertoli. Contraction of myorpithelial cells around toubules. Addition of secretion of seminal vesicles. Prostate and bulbourethral gland. And cilia movement in tubules |
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What causes contraction of myoepithelial cells |
Oxytocin in androgen dependent cells |
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What causes sperm movement in females |
Muscular contractions by oxycoticin. Cilia movement in female tract. Swimming |
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Two processes of sperm maturation in females |
Capacitation. Acrosome reaction |
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Capacitation |
Secretion of female tract allowing for adhesion to ovum and removes proteins from head of Sperm |
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Acrosome reaction |
Factors from ovum ruptures sperm acrosome causing the release of proteolitjc enzymes that break down ovum membrane |
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Layers of uterus |
Endometrium. Myometrium |
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Oviduct |
Tube that connet flopian tube to urterus |
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Parts that are at the entrance to the uterus |
Cervical canal. And cervix |
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Antrum |
Space that occurs for developing secondary follicle |
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Outer layers of follicle |
Thecal cells. Grabulosa cells then zona pellucida |
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Amount ovum per follicle |
One |
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What happens at ovulation |
The ovum is ejected from folicule |
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What happens to foliculr after ovulation |
Luteinzation |
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Lutenization |
Formation of corpus lutenum |
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Luteolysis |
Death of corpus luteum |
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Corpus albicans |
Scar tissue |
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Steroids of ovary and placenta and corpus luteum |
Estrogen. Progesterone. Androgen |
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Endocrines Peptides of ovary and placenta and corpus luteum |
Relaxin. Inhibin |
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What LH causes in females thecal cells |
Testosterone production |
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What FSH causes in granulosa cells in females |
Transition of testosterone to estradiol which is released to blood |
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Luteal phase in granulosa cell |
Lh causes testosterone and the. FSH turns testerstorne to estrogens and both progesterone are released to blood |
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What estrogen causes in the ovary and follicles |
Growth and development |
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Estrogens effect on uterus |
Prepares endometrium for implantation. Induces progesterone receptors. Induces thin watery mucus. And promotes contractions at term |
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What estrogen causes in breasts |
Growth of ducts and fat deposits |
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Estrogen effect on the female body |
Female configuration. Secondary sexual characteristics. Closure of epiphyseal plates. Protects against osteoporosis |
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Hypothalamo pituitary axis causes from estrogen |
Positive and negative feedback |
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Progesterone effect on uterus |
Decidualization and endometrial secretion. Induce thick sticky mucus. Decrease contractions |
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Progesterone effect on breasts |
Growth of glandular tissue |
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Progesterone effect on hypothalmo pituitary axis |
Negative feedback |
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Inhibin is made in |
Granulosa cell through out menstrual cycle prior to ovulation and during lutral phase |
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What inhibin inhibits |
FSH postly in the pituitary |
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Relaxin is synthesized in |
Corpus luteum and placenta |
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What us caused by relaxin |
Decreases uterine contractility in early pregnancy to prevent abortion. Lossen pelvic joints and soften and dilate cervix |
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Gonadal dysfunction of females |
Pseodohermaphroitism. True precocious puberty |
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When a fetus female goes from primordial follicles to primary follicles |
5 months |
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When amount of folicules peaks |
6 months into fetal development |
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Amount of mature oocytes in adults |
400-500 |
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Amount if polar bodies made to make a egg |
Two |
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Menstrual abnormalities |
Amenorrhea |
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Polycystic ovary syndrome |
Have high lvls of androgens |
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What congenital adrenal hyperplasia causes |
Make external genitalia to form |
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Deficiency of congenital adrenal hyperplasia |
21 hydroxylase |
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XX adrenogenital syndrome |
Psudohermamphroditism causing saddle bag scrotum no vagina |
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Hirsutusm |
Androgen excess causing secondary sexual characterists |
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Period of time that occurs from menstruation to ovulation |
Follicular phase |
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Period of time after ovulation to menstruation |
Luteal phase |
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Phase that effects length of menstrual cycle |
Flollicular phase |
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Hormone peak that causes ovulation |
LH and FSH |
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Hormone drop that occurs for ovulation |
Estrogen |
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Hormone that has most for menstruation |
FSH and estrogen |
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Hormone that peaks after ovulation |
Progesterone |
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What estrogen causes |
Decrease in FSH and increase in LH |
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What high FSH lvls causes at the begining if folliculogensis |
Follicle recruitment |
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What FSH causes in granulosa cells |
Production of estrogen |
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Amount if folicules that are recruited per cycle |
6-12 |
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What happens to the non dominate follicle |
They atrophy and become graffian follicle |
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What rising estrogen lvls cause on hupothslmus |
Increase GnRH causing a surge in LH and FSH |
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What causes decline in estrogen before ovulation |
Graffian follicle stops produceing it |
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What the surge in LH causes |
Progesterone release and plasma activity |
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What progesterone causes |
Corona radiata to separate from granulosr cells stopping inhibition of maturation on folicille |
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Length of time that a ovum is viable for after ovulation |
36 hr |
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Formation of corpus lutrum |
Walls collapse and antral fluid is reabsorbed. Thecal blood vessels invade granulosa cells and antral cavity fills with blood. |
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Corpus haemorragium |
When granulosa layers and antral cavity fills with blood |
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What LH does to granulosa cells in corpus luteum |
Become lutenized. |
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Luteinized |
Full of lipid/ steroids |
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Cells that make up corpus luteum |
80% granulosa. 20% thecal cells |
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How long corpus luteum lasts if not pregnant |
14 days |
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What replaces corpus luteum if not pregnant |
Corpus albicans ( fibrous tissue) |
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What luteinized granulosa cells respond to and produce |
LH and produce estrogen and progesterone |
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What progesterone release causes for uterus |
Growth of endometrium and coiling of its spiral arteries |
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Feed back loop of moderate estrogen and high progesterone |
Long loop negative feed back |
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What causes luteolysis |
Lack of LH and FSH stopping production of steroids |
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What causes menses |
Lack if progesterone |
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What spiral arteries coils cause for menstration |
Imped blood flow causing tissue necrosis |
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What PGs release cause for menstration |
Vasoconstriction leading to further tissue ischemia |
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What necrosis if blood vessels cause |
Hemorrhage and endometrial sloughing which is helped by enzymes |
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Blood and tissue volume lost during menstratiin |
25-76ml each (mostly arterial) |
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What PGs cause for smooth muscle of uterus |
Rhythmically contractions and menstrual flow and cramps |
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Menstrual abnormalities |
Amenorrhea. Oligomenorrhea. Menorrhagia. Metrorrhagia. Dysmenorrhea |
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Amenorrhea |
Absent ovulation due to dysfunction if HPG |
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Oligomenorrhea |
Infrequent light bleeding |
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Menorrhagia |
Prolonged heavy bleeding |
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Metrorrhagia |
Bleeding between periods |
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Dysmenorrhea |
Painful period |
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Effect of estrogen on breasts |
Fluid retention and ductal growth of breasts |
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Progesterone effect on breasts |
Increase fluid retention and lobule growth |
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What occurs to breasts prior yo Mendes |
Odema and swelling |
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Two parts of penis involved in erection |
Corpus cavernosum and corpus sponglosum |
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Type of tissue around the urethra |
Corpus. Spongiosum |
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Blood flow that causes erection |
Pressureizes blood enters and veins constrict |
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Where blood gets trapped in penis |
Corpus cavernosa |
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What causes lubrication in penis |
Parasympathetic activation of the bulbourethral glands |
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What causes ejaculation |
Intense sexual stimulation |
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Where sympathetic impulses cause smooth muscle contractions for ejaculation |
Rhythmicly in bulbourethral glands. Prostate and seminal vesicles. And peristaltic contractions in testicular ductdd rpididimus. Vas defferns and ejqculatory ductv |
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Movement to expel things out of the penis |
Rhythmic contraction in erectial column of penis |
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Color change over erection |
It gets darker |
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Four stages of an erection |
Excitment. Plateau. Orgasm. Resolution |
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What causes excitation in females |
Paradympathetic impulses |
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What occurs during excitment |
Vasocongestion of vaginal walls |
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When peak vasocongestion of vaginal wall occurs |
Orgasm |
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Agging issue with male penis |
Erection takes more time and stimulation and is less firm when fully erect and refractory period is longer |
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Ejaculation volume as men age |
Volume decrease |
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Testicular size during aging |
Smaller and signs of sexual arousal are reduceced |
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What loss of estrogen causes in aging women |
Reduced vaginal flow. Resdudrd Vasocongrstion. Reduced lubrication. And may cause dyspareuria |
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Dyspareuria |
Painful intercourse |
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Effect on vaginal wall of ageing |
Vaginal wall loses elasticity and expansion reduces |
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Sexual arousal signs and aging |
Reduce |
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Endocrine issues with male |
Decreased testosterone causes decrease libido but not impair erection |
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Endocrine issues with female |
Decrease in estrogen dryness of vagina and painful intercourse |
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Neural issue for men and sex |
Impotence. Premature ejaculation |
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Neural issues for females sexuaky |
Anorgasmia (1in14 psychological). Vaginismus. Dyspareuria |
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Time it takes for sperm to get to fertilization site |
30 to 60min |
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What helps sperm move through the cervix |
Glycoprotein channels in the mucus |
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How the egg helps direct sperm |
Chenotactic factors |
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Half identical twins (polar body twining) |
Egg splits on two and each egg I'd fertalized seperatly |
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Causes for infertaikity in men |
Impaired spernatogenesis or seman production. Or impaired testicular or penile function |
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Infertility in females |
Anovulation. Infection. Excess thick mucus |
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When zygote begins mitotic division |
30 hr after fertilization |
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How a zygote enters uterine cavity |
As a morula after 3-4 days |
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Morula |
8 cells |
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When a zygote implants |
7-8 days after fetulization |
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What the zygote survives on till implantation |
Uterine milk secreted by endometrium |
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Trophoblast secretion they increases endometrial permeability |
Estrogen |
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What is made by trophoblast that allows for implantation |
Proteases |
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Tropoblast |
Outer layer of cells around the zygote |
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Blastocele |
Fluid filled pouch around the embryo contained by the teopoblast |
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Parts of embryo during blastocyst |
Yolk sack and amniotic cavity |
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Layers around amnonic fluid |
Chorion amnion |
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When the placenta develops |
5 weeks after implantation |
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What makes up the placenta |
Fetal chorionic frondosumn. Maternal decidual tissue |
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What occurs at plecenta |
Exchange between fetal and maternal blood |
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What maternal decidual tissue does |
Production of glycogon |
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Where maternal blood pools form |
Chorionic excavation |
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What forms chorionic frondosum |
From vascularized chronic villi |
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Tissues that have decidual reaction |
Endometrial proliferation. Vascularization. Glycogen accumulation |
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What makes up the placental barrier |
Endothelial cells of the blood vessels |
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What crosses placental barrier by diffusion |
Oxygen. Co2. Ion. Lipids. Steroids |
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What crosses placental barrier by 're rotor mediated endocytosis |
IgGs |
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What gets amino acids across the placental barrier |
Amino acids |
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How glucose crosses the placental barrier |
Facilitated diffusion |
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Functions of the placenta |
Gas exchange. Nutrient delivery. Antibody delivery. Removal of fetal waste. Secretion of hormones |
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Hormones secreted by placenta |
HCG. hCS. Estrogen. Progesterone |
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What hCG causes |
More progesterone and estrogen from corpus luteum |
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What hCG (human chorionic gonadotropin) is like |
LH in structure and action |
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What secretes hCG |
Syncitiotophs 6 days after fertilization. |
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External use of hCG |
Pregnancy tests |
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How concentration changes for hCG |
Doubles every two days till peak at 10 weeks when the placenta forms. Secondary peak in second trimester |
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Hormones effected by hCG |
Increase relaxin. Decrease LH in mother. Increase DHEA in fetus. Decrease mother immune function |
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Why a mother's immune function in decreased during pregnancy |
To avoid abortion |
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What hCS is like |
GH in structte and action |
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What hCS is produced and where it is found |
Syncitiotrophs 4 weeks after implantation. Mainly in maternal circulation |
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Amount if hCS is proportional to |
Placenta size |
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What hCS causes |
Direct nutrients to the fetus induceing a diabetic like state in mother |
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Steroids that the placenta produces from the fetoplacental unit |
Pregnenalone and progesterone from materinal cholesterol |
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What happens to placental prrgnenalone |
Enters fetus and gets turned to androgens |
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Where fetal androgens go |
Into placenta and get converted into estrogen and get passed to mother |
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Concentration change of progesterone over pregnancy |
Increases to term |
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What progesterone causes in zygote |
Division |
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Concentration change of estrogen over term of pregnancy |
Increases to term |
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What causes cervical ripening at parturition |
Relaxin and prostaglandin |
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Parturition |
Term (270 days after fertilization) |
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Parts of myometrial contractions |
Braxton hicks. Labour. Amniotic rupture. Cervical dilation. |
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What stimulates nyometrial contractions |
Oxytocin and prostaglandin |
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How oxytocin causes effects if concentration does not drastical increase at term |
Uterus becomes more sensative due to receptor upregulation |
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How Labour can be triggered with out hormones |
Once a critical size is reached the movement of the fetus triggers contraction |
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Tubal/ectopic pragnancy |
Occurs in oviducts or outside uterus |
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Psudopregnancy |
Emotionaly disturnbed and appear to be pragnant |
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What prolactin causes in breasts |
Sysnthesis of milk in alveoli |
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What oxytocin causes in breasts |
Secretion of milk from avleoli ducts |
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Chiari frommel syndrome |
Persistent, inappropriate lactation |
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Infertility |
Antigonadal actions of prolactin |
