Reproduction 2- Female Reproductive and Pathology Flashcards Preview

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1
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A: An ovary has a [1º Follicle= 1 oocyte surrounded by a cluster of granulosa cells]= [Germ cell surrounded by endocrine tissue]. Follicle is responsible for:

  1. Nurturing and Maturing the resident oocyte
  2. Preparing Vagina & [Fallopian tubes] for fertilization
  3. Prepare uterine lining to accept/implant zygote
  4. Maintain hormonal support for fetus until placenta develops

B: # of oocytes in a female constantly declines AFTER birth due to [continued ATRESIA] but during 1st [20-24 week gestation] germ cells make oogonia via Mitosis.

B2: In this [20-24 week gestation] some oogonia start prophase of meiosis –> [1º oocytes] and arrest there UNTIL ovulation 12-40 years later. {by 6 months after birth ALL oogonia—> [1º oocytes]}. In prophase no other divisions occur and this is when [Atresia] begins.

C: Follicle Development follows 8 Steps
1st. Primordial follicle = inactive oocyte surrounded by [Follicular and stromal cells]

2nd. 1º follicle
3rd. [2º “vesicular” follicle]
4th. [MATURE Graafian Follicle]

5th. OVULATION

6TH.[Corpus Luteum yellow body] forms
7TH. [Corpus albicans] forms
8TH. [atretic follicle] forms

2
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Follicle Development follows 8 Steps

1st. Primordial follicle = inactive oocyte surrounded by [Follicular and stromal cells]
- ————————————————————————————-
2nd. [Primordial follicle-Follicular cells] differentiate into granulosa cells and the oocyte enlarges = [1º follicle]. 1º follicles also have [Zona pellucida] forming. (this process REQUIRES FSH and Estrogen)
- ————————————————————————————-
3rd. [2º “vesicular” follicle] will begin to develop under FSH influence. Cohort of [1º follicles] all become [2º vesicular follicles] and then ONE [2º vesicular follicle] BECOMES [MATURE Graafian Follicle]
* *[2º vesicular follicle] obtain a [Fluid filled Antrum] in center(with FSH & Estradiol)

ºform [Theca EXTerna]

º[2º vesicular follicles] are when [FSH/LH/Androgen/Estrogen] receptors develop on [granulosa cells]

ºFollicle starts to produce steroids

4th. [MATURE Graafian Follicle] come from 1 Lucky [2º vesicular follicle] under FSH influence. It’s [Fluid filled Antrum] enlarges and a [Cumulus oophorous] forms. This [MATURE Graafian Follicle] exponentially grows with large amounts of Antral fluid.

As growth continues [Mucopolysaccharides DePolymerize], granulosa cells in [Cumulus oophorous] loosen up and [Antral Fluid Osmotic Pressure INC]—–>OVULATION

[FSH/LH/Estradiol] are REQUIRED for [MAX Progesterone] and normal growth in a [MATURE Graafian Follicle]. {{Premature LH—>No Mitosis and No Steroid synthesis}}

3
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Follicle Development follows 8 Steps

6TH. [Corpus Luteum yellow body] forms from left over [Granulosa and Theca cells] inside the [ruptured Graafian follicle]. LH turns [Granulosa and Theca]–> [Lutein Cells]
-Since basement membrane is proteolysed, blood vessels invade granulosa cells of the [Corpus Luteum YB]

-[Theca cells] undergo leutinization= accumulate [large yellow lipid droplets] / differentiate / hypertrophy

**[Corpus Luteum YB] secretes the MOST Progesterone(formed faster than it can be processed) and provides gonadal steroids for zygote maintenance & implantation.
Later, Placenta takes this role.
*10 days after formation, NO [fertilization/HCG from IMPLANTED embryo], loss of LH causes [Corpus Luteum YB] regression/luteolysis
—> [fibrous scar tissue = Corpus albicans]
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7TH. [Corpus albicans]= fibrous scar tissue tht forms from regression/luteolysis of [Corpus Luteum YB]
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8TH. [atretic follicle] forms

4
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A: GnRH is a [10 Amino Acid Hormone] that comes from [MOSTLY hypothalamic POA nc.] AND [some hypothalamic arcuate nc.]. It’s release from the [arcuate nc.] can be BLOCKED BY:

1) Dopamine
2) Endorphins
3) CRH

But NorEpi stimulates even more GnRH from [hypothalamic arcuate nc.]
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B: FSH= stimulates follicular development AND [E2 Estradiol Secretion]
vs.
LH= Leutinization and Ovulation

C: Follistatin is secreted BY Gonads and binds up [Gonadal ACTIVIN] while also BLOCKING [ANT Pit Gonadotrope] release of FSH and LH for negative feedback
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D: [Gonadal ACTIVIN] only feedback on [ANT Pit Gonadotrope] to stimulate it–> MORE FSH and LH
vs.

[Gonadal inhibin] feedback on BOTH [ANT Pit Gonadotrope] and [hypOthalamus] to turn them off!
-inhibin A comes from [Corpus Luteum YB]

-inhibin B comes from [Mature Graafian follicle] = [inhibin B] also PARACRINELY augments [Theca Cells] to produce Androgens which remain constant until end of follicular phase in which Androgens slightly INC possibly for INCREASING libido for Ovulatory phase

  • [inhibin A and B] levels are relatively LOW during [Ovulatory phase]

*Both [Gonadal ACTIVIN] and [Gonadal inhibin] are stimulated by FSH. *

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A: [Clomid clomiphene] is a [hypOthalamic estrogen receptor modulator] that prevents estradiol (coming from granulosa cells) from negatively feeding back on hypOthalamus—> [INC pulsatile frequency of GnRH] to stimulate [ANT Pit Gonadotropes]

A2: [Clomid clomiphene] does this by binding to Estradiols hypOthalmic receptor and subsequently recruits REPRESSOR PROTEINS—> represses gene that’s needed for Estrogen negative feedback

A2: [Clomid clomiphene] is a part of a group called SERM= [Selective Estrogen Receptor Modulators] along with Tamoxifen (which treats hormone-responsive breast CA).

6
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MENSTRUAL PHASES: [Follicular–>Ovulatory–>Luteal]
1st: Follicular phase = “variable phase” in which follicle grows. Interval from onset of menses to ovulation.
ºhypOthalamus secretes GnRH–>FSH/LH–>Developing follicle—> Estradiol which [INC follicle development more] and (along with [Gonadal inhibin]) negatively feedback on [ANT Pit Gonadotropes] to DEC FSH

*Estradiol AND inhibin MAY potentially negatively feedback on hypOthalamus as well

ºTHIS NEGATIVE FEEDBACK from Estradiol and [Gonadal inhibin] does NOT shut down FSH/LH release, but just maintains the “volume” as the [Follicle capacity INC]—> LH and Estradiol continue to rise during this phase and hypothalamus sustaining exposure to high levels of Estradiol switches Estradiol from negative to Positive feedback . Estradiol concentration passes a threshold—> LH Surge!

-The Vagina during this phase becomes large, cornified and squamous with small/absent nuclei

7
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MENSTRUAL PHASES: [Follicular–>Ovulatory–>Luteal]
2nd: Ovulatory Phase= Short (1-3 duration) and time oocyte finally matures and is released into peritoneal cavity

º LH surge (determined by ovary) from E2 passing its threshold{Above 200 pg/ml for 36 hours} —>Follicle rupture and this causes sudden drop in E2.

B: Loss of E2 positive feedback during the “drop” DEC LH to new VERY LOW plateau. Remaining follicle forms [Corpus Luteum YB]–> E2 ad Progesterone

C: During Ovulatory Phase E2 and LH still reinforce each other and [inhibin A and B] sum is low

D: During LH surge small rise in progesterone may help the LH surge and (with estradiol) also promote a FSH surge. FSH surge is needed to activate [new cohort of follicles for next cycle]

8
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MENSTRUAL PHASES: [Follicular–>Ovulatory–>Luteal]

3rd: Luteal Phase= Formation of [Corpus Lutem YB] and secretion of hormones for implantation. This is less variable and last 14 days. Pregnancy prolongs the Luteal phase —> Progestational phase.
- Progesterone and E2 NOW both NEGATIVELY FEEDBACK on any GnRH/FSH/LH release

-Luteal phase is dominated by progesterone and vagina during this phase has [basophilic cells with many leukocytes]
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B: Endometrium degrades when there is no [fertilized IMPLANTED embryo making HCG] + loss of LH —>[Corpus Luteum YB regresses]—> E2 and Progesterone levels DEC = Endometrium degrades/sloughs—-> “withdrawal bleeding”/menses

C: During Menses, Estradiol and Progesterone levels are low because [Corpus Luteum YB] has regressed and [new cohort of follicles] are still immature

9
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A: GnRH Tonic mode= found in males and is low with pulsatile LH release

B: GnRH SURGE MODE= found in FEMALES and is periodic MASSIVE RELEASE OF LH
B1) LH surge in females start at puberty (since this is when hypOthalamic surge center matures) and occurs only at night.
–Eventually after menarche LH pulsatility prevails throughout 24 hour period but changes according to phases of monthly cycle

C: During female childhood [FSH is higher]
º[Adult-Reproductive period= LH is Higher]

ºSenescence= FSH is higher again]

10
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A: [Resistant Ovarian Syndrome] = Low Estrogen OR Ovarian receptors are INSENSTIVE to LH and FSH–> a bunch of [primordial follicles] that NEVER develop into [1º follicles]

B: [Estradiol E2 from [MATURE Graafian Follicle] Actions]

  • STOPS Growth of other cohort follicles
  • Positive GnRH feedback–>LH Surge
  • Prepares uterine endometrium for progesterone
  • Prepares Fallopian tube for ovum/zygote transport
  • Alters cervical mucus to enhance sperm mvmnt
11
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*2 compartment theory of [MATURE Graafian Follicle] Steroidogenesis

1st: Since [Theca cells] are highly vascularized they have access to MORE circulating cholesterol. They send this Cholesterol to [Granulosa cells]
2nd: Granulosa Cells make [progesterone & pregnenolone] from [Theca Cell Cholesterol] OR [acetate cholesterol] and will send [progesterone & pregnenolone products] to [Theca cells]
3rd: LH stimulates [Theca cells] to make androstenedione, which diffuses back into [Granulosa Cells]
4th: FSH stimulates [Granulosa Cells] to turn [androstenedione from [Theca cells]] —>[Estrogen with its Aromatase] and Testosterone

B: Since [Theca cells] are highly vascularized they have access to circulating cholesterol. They send this Cholesterol to [Granulosa cells] to be converted into progesterone & pregnenolone] vs. [Granulosa cells] which can only get Cholesterol from acetate.
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C: Theca cells don’t have Aromatase to make Estradiol

12
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A: Endometrium growth and development is described with 
Proliferative Phase
vs. 
Secretory phase
vs. 
Menses
  1. Proliferative phase= [estradiol dominated] and coincides with mid-to-late follicular phase
    ºThickening of stromal & endothelial layers

ºVascularization w/spiral arteries

ºINC in progesterone and estrogen RECEPTORS

ºConstant Basal body temperature

13
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A: Endometrium growth and development is described with 
Proliferative Phase
vs. 
Secretory phase
vs. 
Menses
  1. SECRETORY PHASE occurs from [Ovulation Day] to [Late Luteal Phase] right after [Drop in Basal body temperature].
    ºVascularization INC but with Glycogen content INC as well

ºEndometrial glands secrete Carb-rich mucus for secretions

ºStroma becomes Edematous

º[characterized by a (0.5ºC) INC in Basal body temperature]

14
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A: Endometrium growth and development is described with 
Proliferative Phase
vs. 
Secretory phase
vs. 
Menses
  1. Menses= low estrogen and progesterone levels
    ºRestriction of spiral arteries–>ischemia, necrosis and rupturing of blood vessels

ºINC proteolytic enzymes with infiltrating leukocytes
–>Digest tissue

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A: Estrogen in the Follicular phase INC the amount, alkalization and Viscosity of the Cervical Mucus

  1. [Spinnbarkeit stretchable mucus]= found RIGHT BEFORE OR DUING OVULATION
    * **[Ferning]= Characteristic PATTERN tht Occurs when you Dry [Spinnbarkeit stretchable mucus] on glass slide

B: These changes promote sperm survival and transport and are a primitive test for ovulation

16
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Menopause= loss of negative feedback from estradiol and inhibin—>Pulsatile release without cycles.

Consequences
1. Osteoporsis= INC bone ReSorption

  1. [CV Dz-Atherosclerosis]= INC cholesterol, [INC LDL w/dec LDL receptors]
  2. Thinning of Vaginal epithelium and DEC secretions/breast mass
  3. Vascular Flushing= “Hot Flashes”= INC vasomotor activity that synchronous with LH pulses—>periodic INC in core temp / sweating / pulse rate / reflex vasoDilation
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WOMEN HEALTH INITIATIVE RESULTS
A: CAD INC in combined treatment (Estrogen and Progesterone)

B: Stroke SIGNIFICANTLY INC in Estrogen therapy but regularly INC with combined tx (2º to INC in Venous thromboemobolism). = stopped early

C: Breast CA had slight benefit from Estrogen therapy but INC with combined tx

D: Osteoporosis DEC for both

E: Colorectal CA DEC risk for [combined tx] but no change with [Estrogen alone]

  1. One thing to keep in mind is that Women have to receive [Hormone Replacement Therapy] around same time they START menopause. Starting after 10 years–> detrimental outcomes = [TIMING HYPOTHESIS]
18
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A: [1º Amenorrhea]= absence of menses in phenotypic female by age 17

Causes:

  • Turner Syndrome
  • [Complete Androgen Resistance]/Testicular Feminization
  • Hormonal Disorders in ovaries/Adrenals/Thyroid/Pituitary
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A: [2º Amenorrhea]= Menarche has occurred BUT HAS STOPPED and for longer than 6 months

Causes:

  • PREGNANCY IS MOST COMMON CAUSE
  • Lactation
  • Menopause
  • Hyperprolactinemia 2º to [ANT Pit Lactotrope tumor] or excess GH. Prolactin DEC GnRH pulsatile frequency from hypOthalamus and DEC LH/FSH
20
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A: Oligomenorrhea= infrequent periods with cycle length greater than 35 days

  • Commonly caused by changes in CNS that regulate [GnRH release] like from stress & illness
  • low body fat composition

*Intesnse exercise (anorexia nervosa)–> No consistent change in plasma gonadotropin or ovarian steroid
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B: DYSmenorrhea
Painful menses related to uterine contractions and pelvic pain that radiates to back and thighs (accompanied with N/V).
-Caused by Prostaglandin synthesis promoted by E2-. Prostaglandins may actually cause ischemia
Tx= Oral contraceptives and Prostaglandin inhibitors

21
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A: Hirsutism= HEAVY hair growth in Androgen sensitive areas! caused by taking exogenous androgens or excessive androgen production by Adrenals (such as

  • [Congenital Adrenal Hyperplasia]
  • Cushing Syndrome
  • Virilization= clitoral hypertrophy/ deepening voice/ temporal balding

OR

INC Idiopathic INC in sensitivity to androgens
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————————————————————————————
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B: [PreMenstrual Syndrome] occurs in [late Luteal phase] of 30% of normal cycle females.
Sx= [abd bloating]/ fatigue/ breast tenderness/ irritability
*Cause NOT CLEAR! but Tx= AntiDepressants and ovulation suppressants

22
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A: [Polycystic Ovarian Syndrome] = mostly caused by/causes of Insulin Resistance and Obesity (which are actually causes AND caused by..]. Will cause infertility

ºHigh insulin stimulates androgen production—> infertility AND [INC conversion to estrogens= wt. gain]

ºFollicle development becomes impaired from High Androgens and ovulation isn’t completed–>Follicles degenerate into cyst –>ovaries double in size

B: Sx= [sleep apnea] / menstrual irregularity / obesity/ DEC HDL / Hirsuitsm

C: Tx= include wt. loss, smoking cessation, [metformin(for insulin resistance) which is sufficient to restore fertility]. [Clomid Clomiphene is also effective]

23
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AKA= [[Peak fertility is between ages 18 - 25]] and Infertility QUADRUPLES between 20—>40!

B: Fertilization (which occurs within 24 hours after ovulation) requires RAPID transport of germ cells to oviduct since ovum are only viable for 12-24 hours.

C: Gestational age is calculated from 1st day of LAST MENSTRUAL PERIOD.

[FETAL AGE= (Gestational Age) - 2 weeks ]

D: Best Ovulation window is [24 hours post ovulation for ovum] and [2-3 days post Coitus for Sperm]

E: When Fertilization does actually occur, Embryo implants into endometrium and placenta is formed with both fetal AND maternal cells.

  • Placenta will act as new ENDOCRINE GLAND for steroid/protein hormone production—> Sx of Pregnancy= (Breast tenderness / fatigue / nausea / [sustained elevated body temp] / amenorrhea )
  • Placenta also is needed for Resp/Kidneys/Nutrients/(MOST Viruses can cross placenta)
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A: [Sperm Capacitation] describes changes in spermatic functional properties tht occur in female tract and allow sperm to penetrate [Zona Pellucida]

-Vagina removes and modifies spermatic protein coat

B: Acrosomal Rxn= Release of [HAN Acrosomal enzymes]= [Hyaluronidase/ Acrosin / Neuraminidase] that disperse [granulosa cells] and allow sperm to attach to zona pellucida and penetrate
*Spermatozoan bind to [Granulosa ZP3 glycoprotein receptors]—>IP3—>[INC intracell Ca+]—>fusion of outer and inner membranes—>[enzyme-rich internal membrane contents diffuse out of sperm] onto ovum

25
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C1: **Once Sperm Acrosomal Rxn occurs, Spermatozoan penetrates [Zona Pellucida] which

  1. triggers exocytosis of oocyte internal vesicles
  2. INC Ca+ –> fusion of cortical granules w/membrane –> harden/cleaves [Zona Pellucida Glycoprotein receptors].
  3. completion of oocyte’s SECOND MEIOTIC DIVISION pulling it out of Metaphase 2

C2: After hardening [Zona Pellucida] (to prevent POLYSPERMY) Spermatozoan and Ovum plasma membrane FUSE TOGETHER —> [Sperm Nucleus] enters egg cytoplasm

D: completion of oocyte’s SECOND MEIOTIC DIVISION will pull it out of Metaphase 2–>release of the 2nd polar body –> leaving an oocyte with haploid unduplicated chromosomes that will fuse with male pronucleus —> Zygote

26
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SPERM TRANSPORT
A: Sperm Transport within cervix [post coitus] last for 1-3 days and sperm retain their fertilizing capacity for 1-2 days (optimal time for fertilization is within 24 hours of ovulation). DESPITE THE 250 MILLION THAT ENTER, ONLY A FEW HUNDRED MAKE IT TO AMPULLA/[OVIDUCT FALLOPIAN TUBE]

B: Estrogen during [late follicular phase] primes female tract to help in sperm transport
-Secretes cGMP to INC velocity & direction of sperm

  • INC Vagina pH
  • DEC Viscosity of cervical mucus–> [Spinnbarkeit stretchable mucus]

-INC ciliary mvmnt/ peristaltic mvmnt/ fluid flow in oviduct
————————————————————————————
OOCYTE TRANSPORT
1. At ovulation, oocyte with its [Cumulus Oophorus] is released into peritoneal cavity and swept into [oviduct fallopian tube] by fimbriae .
2. Ampulla contraction produces churning motion that promotes random encounter between sperm and ovum

27
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Once the Zygote has formed—>Morula which traverses the [Oviduct fallopian tube] for 3 days. Arrival of Morula in uterine cavity depends on progesterone vs. estrogen balance

A: Estrogen stimulates [isthmus contraction] which creates [utero-tubal passageway] for embryo–>uterus BUT ALSO delays transport at the [utero-tubal junction] so that endometrium has time to develop

B: Later, Progesterone INC and promotes myometrium relaxation and actual transport of Morula to uterus.

C: Egg enters uterine cavity as a Morula and implants on Day 7 post-fertilization—>Blastocyst

28
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Implantation of Blastocyst requires

  1. Adhesion—> 2. Penetration and then 3. Invasion
    * *This process has a 70% Failure Rate!

Adhesion
1st) Zona Pellucida dissolves/Egg hatches (REQUIRES Progesterone from luteal phase) and Integrins in both tissue (developed by Blastocyst IL-1) bond endometrial cells together and blastocyst cells together

2nd) OsteoPontin binds Integrins of endometrium and blastocyst together—> TROPHOBLAST which is connected to endometrium via [laminin & fibronectin]

29
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Implantation of Blastocyst requires

  1. Adhesion—> 2. Penetration and then 3. Invasion
    * *This process has a 70% Failure Rate!

PENETRATION
Involves [Trophoblast Microvilli] interdigitate with endometrial cells and then trophoblast burrowing under epithelial cells while phagocytizing dead endometrial cells

B: [Fibroblast-like Stroma Cells] are stimulated by Progesterone to enlarge and form the [Decidua]. These cells give nutrients to embryo while vascular connections are being developed AND are a mechanical/immune barrier.

30
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Implantation of Blastocyst requires

  1. Adhesion—> 2. Penetration and then 3. Invasion
    * *This process has a 70% Failure Rate!

INVASION
A: Balance between [Decidua Cells= Defense] and [Trophoblast migration= Offense]. [Trophoblast migration cells] secrete [Matrix MetalloProteinases MMP] and [IGF2] to start invasion.

B: [Decidua Cells] secrete MMP Inhibitors and [IGF2-Binding Protein] which’ll prevent invasive trophoblast from penetrating too deep.

31
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TROPHOBLAST CAN DIFFERENTIATE INTO:
1) Syncytiotrophoblast= mass with NO cell boundaries and extends between uterine epithelial cells. Secrete TNF into basement membrane and responsible for MOST ENDOCRINE. These are surrounded by [Decidual cells] which provide nutrients.

vs.
2) Cytotrophoblast= secrete [hypOthalamic-like stimulatory hormones such as CRH, TRH] and [inhibitory (somatostatin) proteins] that act on Syncytiotrophoblast = [intrauterine hypOthalamic-Pituitary axis].

B: **Cytotrophoblast causes release of GnRH
—>Syncytiotrophoblast to produce HCG. This HCG signals to maternal ovary that implantation has occurred and begins Luteotrophic process (saves corpus luteum YB).

***HCG (along with inhibin) also negatively feeds back on [ANT Pit Lactotropes] to prevent LH/FSH secretion that would otherwise stimulate new cohort of follicles to develop.

C: Steroid hormone production requires [feto-placental unit]

32
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A: Thick layer of well vascularized endometrium is ideal for embryo implantation in the [Luteal phase-Secretory]

B: Menses/sloughing typically takes 4 days to completely remove endometrium
————————————————————————————
C: In the transport of Nutrients across Placenta
[Glucose/ AA/ electrolytes] can diffuse or facilitated diffusion
vs.
Oxygen can diffuse down concentration gradient. Fetal HgB has higher affinity for O2

D: Waste (Urea Creatinine) is also removed in Placenta and pCO2 in fetal arterial blood is 2-3 mmHg HIGHER than maternal blood–>ALLOWS CO2 TO DIFFUSE DOWN ITS GRADIENT INTO PLACENTA

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A: Lab Antibodies targeted against [HCG-Beta subunits] are used in radioimmunoassays for pregnancy test. [HCG-Beta subunits] can be found in maternal urine 9 days after conception.

B: **Cytotrophoblast causes release of GnRH
—>Syncytiotrophoblast to produce HCG. This HCG signals to maternal ovary that implantation has occurred and begins Luteotrophic process (saves corpus luteum YB).

***HCG (along with inhibin) also negatively feeds back on [ANT Pit Lactotropes] to prevent LH/FSH secretion that would otherwise stimulate new cohort of follicles to develop.

C: [Human Placental Lactogen (HPL) or Human Chorionic Somatomammotrophin (HCS)] is structurally similar to growth hormone and is released during [pregnant hypOglycemia].
C2: HPL INC lipolysis and has ANTI-insulin actions on maternal carb metabolism—–> INC plasma glucose and FFA in order to maintain flow of these nutrients to the fetus.