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80 Cards in this Set
- Front
- Back
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Pelvic differences between F and M
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Transverse diameter wider, pelvic arch wider, pubic bones longer.
Reflect function - childbirth |
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Where do gonads develop from?
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Gonadal ridge from the intermediate mass of mesoderm (also kidneys and adrenal derived from this)
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Gonocytes
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Germ cells
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Pregnancy requirements
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Fetal resp.
Nutrition, excretion Growth : expanding uterus Development - maintaining corpus luteum, progesterone Control placental blood flow Uterine partial quiescence during development Prevent immune rejection of fetus Control hormones reaching fetus Transmit immunoglubulins to fetus Fetal control of maternal metabolism Placental production of estrogen to affect maternal uterus/breast |
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Functions of trophoblast
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Physical attachment
invadision of endometrium transfer resp gases Transfer of nutrients and waste products Synth of hormones Synth and breakdwon of other substance - esp. proteins Immunological barrier - prevents maternal rejection |
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Role of Estrogen in pregnancy
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Uterine growth
preparation for parturition by; -inducing production of cotraction associated proteins by myometrium, oxytocin receptor production, and increases excitability of myometrium) preparation for lactation - stimulates development of the duct system of the mammary gland. Estradiol from DHEA from fetal adrenal, placenta converts it (because doesnt have enzymes for cholesterol to estradiol |
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Pregnancy duration and phases
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40 weeks - 3 trimesters
phases; preimplantation 7-9 days after ovulation Embryonic - up to 8 weeks Fetal - 8 weeks to term |
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Function of the hormones of the fetal-maternal-placental unit
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maintain pregnancy
control growth influence maternal metabolism prepare for parturition prepare for lactation suppress further ovulation |
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Stages of placental development
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Previllous embryo - no villi, cytotrophoblast covered with syncytiotrophoblast.
1y villi: defined cyto projections covered with syncytio 2y villi: mesenchymal core - within the cyto 3y (true) villi: mesenchyme invaded by fetal (allantoic) blood vessels Further dev - branching of villi (inc SA), thinning incomplete cyto and marginal vessels |
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PLacental blood flow
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Intervillous spaces receive blood from umbilical artery(from int. iliac) branches varrying DEOXYGENATED blood.
Oxygenated, nutrient rich blood from the placenta enters via the umbilical vein to the liver (through-passed by the ductus venosus) and from there to the right atrium. Blood enters the intervillous space from the spiral arteries Countercurrent flow in intervillous space to assure max. transfer Blood leaves intervillous space by uterine veins. Uterine contractions spurt arterial blood in and close venous outflows - increasing pressure |
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Placental growth and efficiency
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Placenta grows during pregnancy, however fetus grows relatively faster.
Therefore palcental efficiency must increase to supply fetus ( this is the problem with late born babies) -inc branching of villus and formation of brushborder on syncytiotrophoblast for inc exchange -thinning of villus to inc SA -thinning placental barrier - endothelium and BL of fetal capillary, stroma of villus (decreases to nothing), basal lamina of cytotrophoblast, and syncytiotrophoblast (big decrease in thickness. |
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PLacental transport mechanisms
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Simple diffusion
Carrier mechanisms (receptors on brush border of syncytiotrophoblast) for immunoglobulins, or for concentrating certain things like metal ions, glucose, vitamins, AA's and some hormones. |
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Progesterones role in pregnancy
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Maintains uterine quiescence
Causes formation of alveoli in breasts -supresses milk production |
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How does fetus avoid immune rejection?
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Fetus expresses both maternal and paternal genes - why not rejected as allograft?
E=skin transplantation experiments show the maternal immune system does function during pregancy...trophoblast at interface - how avoid destruction? -antigens of paternal origin not expressed on interface -trophoblast secretes some progesterone and hCG that suppress immune response -Main mechanism=IDO (an enzyme) expression (by Villi of trophoblast) which rapidly breaks down tryptophan - which is necessary for T-cell activation. E=if inhibited = pregancies rejected. |
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Placental abnormalities
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Abnormal implantation site
Placental insufficiency (as caused by smoking - vasoconstriction) fetal malnutrition, growth retardation -Hydratiform mole - non invasive tumour of the trophoblast - paternal imprinting - 2 sperm - no female pronuclei) |
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Role of amniotic cavity
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mechanical buffer
route of excretion |
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Why corpus luteum need be maintained?
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Progesterone provision - essential for pregnacy (E=block receptors - terminates pregnancy) hCG keeps it alive
Also acts locally in placenta to activate steroidogenesis |
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Fetal growth
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Places considerable nutritional demands on mother
Progesterone - stimulates appetite and alters deposition of fat reserves Placental lactogen - increases free fatty acids available by changing mothers metabolism. Epidemiological studies have shown that, provided adequate nutrition is available to mother, energy balance regulated to provide a fetus appropriate to mothers body size. Fetal length affected by fetal growth hormone, size by IGF2 |
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Fetal malnutrition
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Effects adult pathology - High BP, diabetes mellitus (type 2), and Coronary heart disease. Underweight babys have reduced life expectancy.
Partly due to long term programming of glucocorticoid stress axis, which becomes chronically overactive. |
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How does uterus maintain quiescence
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When smooth muscle of uterus stretched it doesnt contract as you would expect - why?
-uterus grows at same rate as conceptus,so little stretching occurs before very late pregnancy. -progesterone vital for quiescence. Increases in level during pregnancy - acts on muscle cells directly, on chorionic enzymes which prevent prostaglandin accumulation that would activate myometrium, and, reduce oxytocin receptor quantity on uterine muscle cells -Prostaglandin produced is primarily P1 which is a relaxing prosta Oestrodiol main hormone causing uterus growth (however also causes inc in contraction associated proteins and oxytocin receptors to prepare for parturition. |
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Essentials of parturition
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Generation of contractile machinery in uterine muscle
Timing - with fetal maturation changing smooth muscle from quiescent, non-coordinated state to contractile, coordinated state Changing cervix to be able to distend sufficiently |
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Hormones associated with parturition
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Estradiol - inc excitability, inc Oxytocin receptors, in contraction associated proteins.
Prostaglandins to stimulate contractions and ready cervix Estrogen and progesterone to prepare for lactation |
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Signals for parturition
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some random contractions but dont cause birth because not coordinated)
E=early evidence provided by sheep that ate weed which made them deliver grossly over term. Fetus were anencephalic. Without Hypothalamus, CNS cant signal to ant.pit that stress levels high, no ACTH therefore released, so fetal adrenal produces no DHEA sulphate, so none converted to estradiol and progesterone by placenta. Proved by injecting glucocorticoids - caused parturition - showed this was by change estrodial/progesterone ratio within uterus causing contraction. Slightly different in humans as progesterone does not fall significantly at term. Also major difference that placenta makes CRH, rises towards term, glucocorticoids inc placental CRH secretion and therefore DHEA-S production and therefore inc estrogens. Although ratios dont change, inactivation of intracellular progesterone receptors - favours estrodiol action, prostaglandin and gap junction formation that coordinates contractions. Also Oxytocin cells become coupled and can fire synchronously. |
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Parturition involves +ve feedback loops
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Ensure contraction proceeds until uterus completely emptied.
Stretch receptors of cervix (due to babies head - sensory fibres to hypothalamus - Oxytocin release. Acts on receptors to cause more contraction, further stretch - +ve feedback Also contractions and stretch also cause synth of more contractile prostaglandins - creating a further loop. Loops only broken if uterus rupture or child born. |
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Parturition - 3 stages
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contractions cause cervix to dilate so fetal head can pass. Amniotic sac ruptures (waters breakind)
2nd stage: deliver baby and 3rd birth of placenta. |
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Other prep for postnatal life
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Surfactant on lungs to allow to expand with first breath
Changes to gut and liver enzymes to allow for milk digestion (changes induced by glucocorticoid secretion - increase markedly towards term) |
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Lactation
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Mammary gland development via prog, estr, and placental lactogen.
12-20 galactopoeitic (milk producing) lobules Maintainance of lactation by suckling which causes Prolactin (stimulates synth and secretion of milk constituents) release Milk ejection (via contraction of myoepithelial cells surrounding alveoli) stim by oxytocin. (Lactation requires that estrogen and progesterone levels fall First milk produced contains an abundance of IGA antibodies, protect fetus from local infections. |
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Lactation suppresses pregnancy
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Suckling inhibits GnRH release from hypothalamus.
Prevents the excessive metabolic demand another pregnancy would place on mother. |
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Sites of fertility treatment
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Assistance or barrier at;
-brain -pituitary -testis/ovary -epididymis/oviduct -vas/uterus -seminal vesicles and prostate/vagina |
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(Fertility) Brain
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Use GnRH to test pit. function
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MOrning after pill
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Large dose of progesterone;
-prevents ovulation, and/or; -prevents implantation and/or -thickens cervical mucus to reduce/prevent sperm penetration |
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For fertile gamete transmission need;
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Correct chromosomal complement.
Fuctioning gonada Behavioural sex Correct int. and ext. genitalia |
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XX males?
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Translocation of the testis determining part of the Y chromosome (short arm of Y chromosome)
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XY females?
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Deletion of SRY gene
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SRY gene codes for?
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DNA binding protein - triggers male development.
E=Transgenic mice with SRY = phenotypic males |
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Gonad development
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Develop from intermediate mass of mesoderm - form gonadal ridge.
CE:failure of ridge development - mutations in WT1 or SF1 E= knockout = no gonads |
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SRY triggers the Gonadal ridge
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differentiation of mesodermal cells to form sertoli cells - products of which direct the differentiation of the testes with tubules and interstitial cells.
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Where for the germ cells develop?
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Gonocytes develop in epiplast. Migrate to germinal ridge.
Need cell surface receptors. E=no germ cells - still get normal testes in males |
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Internal genitalia.
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Paramesonephric duct develops closely associated with mesonephric duct.
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Paramesonephric duct
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also called Mullerian.
Kept in female to make, uterus, uterine tubes and vagina. Degenerates in males due to presense of AMH from Sertoli cells. E=testis graft and AMH injection |
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Mesonephric duct
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Wolffian. Forms epididymis, Vas deferens, seminal vesicles
Degenerates in females, maintained in males by testosterone from Leydig cells of testes E=implant testosterone also E=uni and bi-lateral castrations, and testis graft |
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External genitalia
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Testosterone converted to more active 5alpha-dihydrotestosterone - masculinises ext. genitalia and prostate.
CE=5Alpha reductase deficiency - Male int. genitalia but female external. However if partially funct enzyme, at puberty - when high testosterone - inc 5alpha DHT so testis descend into labia and clitorus enlarges to penis like structure |
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Androgen insensitivity syndrome (AIS)
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Mutation in androgen receptor
Internal testes, external female genitalia. No uterus, no male ducts. (Still AMH, no testorsterone effect) |
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hCG receptor mutation in XY individual
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hCG stimulates leydig cells to release testosterone. So feminisation of individual.
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Why important that testes in scrotum?
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Temperature - reduces risk of cancer, and infertility
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Gubernaculum
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Descent of testis, attached to apex of testis and scrotal skin, acts as pathfinder.
Preceded by processus vaginalis - part of peritoneum, this becomes tunica vaginalis which surround most of testis. In females does ovary descent to pelvis. Attached around ovary-fallopian junction. |
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21 hydroxylase deficiency
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Because fetal adrenal also causes androgen production. Malfunction can cause masculinisation.
No cortisol secretion (due to deficiency of 21 hydr.) no -ve feedback on ACTH, so increased, so inc DHEA - masculinises fetal female |
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Behavioural sex
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Gonadal hormones effect behaviour
E=female rats - give testosterone - stops estrous cycle and male behaviour occurs E=structural diff between male and female brains. Also difference between straights and gays. |
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Levator ani
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forms pelvic floor (holes for stuff!)
Below it is perineal membrane Pelvic fascia covers it - contains vessels and nerves etc. |
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Perineum
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Space between pubic symphysis and coccyx
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Tunica vaginalis
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Acts like a bursa - allowing free movent in scrotum.
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Spermatic cord
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Passes through inguinal canal (superficial to deep ring)
Components; testicular artery and vein and lymphatics and sympath innerve etc and VAS deferens |
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Vasa efferentia
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from top rete testis to epididymus
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Vas deferens path
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from epididymus, through inguinal canal, then retroperitoneally down side of pelvis
then emedially to end as ampulla between 2 seminal vesicles to join their ducts |
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Prostate
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Beneath bladder, abover perineal memb.
Ducts open alongside urethral crest (ejaculator ducts open onnto crest) |
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Arterial supply and venous drainage of testis and external genitals
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Testis - Gonadal artery, pampiniform plexus of veins drains to IVC and L renal vein
erectile tissue (and seminal vs and prostate) from Internal Iliac |
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Erection
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S2-4 parasympathetic innervation - NO release causes inc cGMP - calcium efflux and therefore relaxation.
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Emission and ejaculation
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Emission=contraction of smooth muscle surrounding Vas and seminal vesicles - sympathetic (T12-L2)
Ejaculation somatic - striated muscle around bulb of urethra (pudendal nerve) |
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Breast tumour spread
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spread from pectoral node - central and axillary nodes - internal thoracic node...
lymph nodes can be blocked by tumour! |
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Male reproductive strategy
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Quantity - increased chance of passing on genetic information
Quality compromised - selection of fittest - in tract Produced by epithelium of seminiferous tubes. |
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Between ST
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Interstitial tissue;
Leydig cells, blood and lymph vesels and autonomic nerves |
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Tunica Albuginea
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Fibrous - ensheaths testis and septa
(further surrounded by tunica vaginalis) |
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Sertoli cells
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Non-germ line, extend from BL to tubule lumen
Tight junction between them to prevent haploid sperm cells crossing testis-blood border and causing immune response |
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Spermatogonia
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Stem cells found in basal compartment (below sertoli cells)
Undergo repeat mitosis to form more stem cells and primary spermatocytes |
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Primary spermatocytes
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Committed to meiosis
Duplicate their DNA, cross through junct. complex and undergo first meiotic divison |
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Secondary spermatocytes
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Undergo 2nd meiotic division forming 4 haploid spermatids.
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Why condense nuclear chromatin of sperm
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Very little haploid gene expression needed
Protects it from damage |
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FSH and LH effects on male reproductive system
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FSH - Stimulates sertoli cells division and their interaction with germ cells
LH - acts on Leydig cells to produce testosterone Testosterone and FSH act together to stimulate onset of spermatogenesis |
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Spermatogenesis end stages
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Spermatids form a tail and develop a thickened mid piece where mitochondria gather to corm an Axoneme. The DNA also undergoes packaging and becomes condensed.
Golgi app. now surrounds the nucleus and becomes the acrosome. One of the cell centrioles becomes the tail. Then Maturation |
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Problems that may arise from incorrect spermatogenesis
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Downs, pataus, edwards
Klinefelters, turners |
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Maturation
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Under infl. of testosterone
Removes unnecessary organelles and cytoplasm. Residual bodies phagocytosed by sertoli cells. Resulting spermatozoa are mature, but non-motile. Released from the sertoli cells into the ST lumen. While in the epididymis the sperm gain motility, although their transport through the remainder of the system is acheived by muscle contraction rather than their motility. |
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Scrotum
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Pouch of skin containing testis epididymis and supporting vessels etc.
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Vas deferens
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Smooth muscle duct with narrow lumen - continuous with tail of epididymis.
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Seminal vesicles
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Produces seminal fluid - Fructose
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Prostate
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Produces fluid rich in acid phosphatase
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oogonia
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Female stem cells - divide mitotically just like male counterparts, but then arrest in 1st meiotic division
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Causes of male infertility
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Heat
Smoking excess alcohol |
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2 functions of ovary
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Haploid gametes and hormone formation
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Secondary sex characteristics
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ie. facial hair male
enlarged breasts female |
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Theca interna
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c.f. leydig cells
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