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555 Cards in this Set
- Front
- Back
|
what 7 factors determine your gender?
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chromosome, gonad, internal genitalia, external genitalia, perceived gender, gender role, sex object preference
|
|
The cortex of the undifferentiated gonad develops into.....?
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the ovary
|
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the medulla of the undiffereniated gonad develops into..........?
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the testis
|
|
what 3 sources are the gonads derived from?
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mesothelial lining of the body cavity, underlying mesenchyme, and primordial germ cells
|
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where do the primordial germ cells come from?
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the yolk sac
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What gene on the Y chromosome is required to spur male development?
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SRY
|
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what does SRY gene do?
|
stimulates an autosome to produce H-Y antigen, stimulates sertoli cells, saves the mesonephric ducts
|
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What does H-Y antigen do?
|
stimulates the medulla of the gonad to turn into a testis
|
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Where is the gene for H-Y antigen located?
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On an autosome. I don't know which one
|
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What does the SOX9 code for?
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collagen II
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People with no functional SOX9 gene suffer from what condition?
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Compomelic Dysplasia
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What does Steroidogenic Factor (SF-1) do?
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codes for androgen synthesis, stimulates MIH from Sertoli cells
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What does the XH2 gene do?
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codes for H type hemoglobin
|
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What does a mutation in XH2 gene do?
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gives a female phenotype to a person with XY genotype
|
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Who is DMRT-1 expressed in, and what happens when it is deleted?
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Only males express DMRT-1, and if it is deleted from the Y chromosome, you have a female phenotype
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If you have a mutated or missing WT-1 gene, what will happen to you?
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You will have undifferentiated streak gonads
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The fibrous capsule of the testis is called the....?
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tunica albuginea
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What 3 structures do the embryonic seminiferous cords develop into?
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seminiferous tubules, tubuli recti, and rete testis
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What is the embryological origin of the Leydig cells?
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the mesenchyme
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What does AMH (also called MIH) do when the testes secrete it?
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supresses development of the paramesonephric ducts (mulerian ducts) which are then reabsorbed
|
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What 3 things are required for correct ovary development?
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absence of functional Y chromosome, migration of germ cells to the gonad, and at least 2 functional X chromosomes
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What happens to the gonads if there is a Y present, no matter how many X's?
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you get balls. One Y counteracts all the X's you could throw at it
|
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What happens to the gonads if there is only one X chromosome?
|
you get streak gonads, no ovaries. sorry.
|
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What one gene is primarily responsible for ovary development?
|
DAX-1
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What happens to the gonadal cords and rete ovarii in females?
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they form, and then are re-absorped
|
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germ cells become ova in females. How many ova does a 20 week-gestation fetus have?
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20 million
|
|
germ cells become ova in females. How many ova does a newborn baby have?
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2 million
|
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How many oogonia form after a female is born?
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None. They all form when you are a fetus
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What is the embryonic origin of the internal genitalia in males?
|
wolffian ducts (mesonephric ducts)
|
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What is the embryonic origin of the internal genitalia in females?
|
mulerian ducts (paramesonephric ducts)
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|
What do the mulerian ducts turn into in females?
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uterus, fallopian tubes, upper 1/3 of the vagina
|
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What do the wolffian ducts turn into in males?
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seminal vesicles, epididymus, ductus deferens
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What hormone stimulates the formation of male parts from the wolffian ducts, and where does it come from?
|
testosterone from the fetal testes
|
|
What hormone gets rid of the mulerian ducts in males?
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MIH, also called AMH
|
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What is the tunica vaginalis?
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Empty sack on the ventral side of each testis. Remnant of the peritoneum
|
|
What two structures does the gubernaculum connect?
|
south pole of the gonad with the inside of the external labioscrotal swelling
|
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In an adult male, where is the ductus deferens inrelation to the ureters?
|
It loops up in front of them, goes over, and then down behind them to connect to the seminal vesicles
|
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Where is sperm stored after it is made in the adult male?
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made in the testicle, stored in the epididymus
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What does the gubernaculum do in males?
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pulls the testes down out of the body, through the inguinal canal, and into the scrotum
|
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What does the gubernaculum do in females?
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pulls the ovaries down into the pelvis, but no further. persists as a cord in adult women
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What undifferentiated structures become the external genitalia?
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genital tubercle, labioscrotal swelling, and urogenital folds
|
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What does the genital tubercle become under the influence of androgens?
|
penis
|
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What do the labioscrotal swellings become under the influence of androgens?
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scrotum
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What do the urogenital folds become under the influence of androgens?
|
external urethra
|
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What do the urogenital folds become without the influence of androgens?
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labia minora
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What do the labioscrotal swellings become without the influence of androgens?
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labia majora
|
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What does the genital tubercle become without the influence of androgens?
|
clitoris
|
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Where does the prostate come from?
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endodermal outgrowths from the urethra form the glands, mesenchyme form the stroma
|
|
Where do the bulbourethral glands come from?
|
endodermal outgrowths from the urethra form the gland part, mesenchyme form the stroma part
|
|
Does female sexual development depend on having ovaries or hormones?
|
NO! it really only depends on lacking androgen influence
|
|
At how many weeks of gestation do the germ cells start to migrate?
|
5 weeks
|
|
At how many weeks do the undifferentiated gonads commit to either testes or ovaries?
|
7 weeks
|
|
At how many weeks do the wolffian/mullerian ducts commit themselves to either male or female parts?
|
10 weeks
|
|
At how many weeks do the external genitalia commit to becoming male or female?
|
14 weeks
|
|
What's the difference between sex and gender?
|
no hard line, but sex tends to refer to physiologic things, while gender refers to cultural or psychological things
|
|
Define intersexuality
|
disagreement between 2 of the organic sex criteria
|
|
Define transsexuality
|
disagreement between 1 organic sex critera and 1 psychological gender criteria
|
|
What is the prevalance of children born intersexed?
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1 in 2000
|
|
what percentage of intersex children have congenital adrenal hyperplasia?
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98%
|
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Individuals with only 1 sex chromosome (YO) are said to have.....?
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Uh, death. You can't live without an X chromosome
|
|
Individuals with only one sex chromosome (XO) are said to have......?
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Turner's syndrome
|
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What are some classical signs of a person with Turner's syndrome?
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short, webbed neck, broad chest, wide inverted nipples, coarctation of aorta, bicuspid aortic valve
|
|
What do Turner's Syndrome babies look like at birth?
|
normal females
|
|
What do the gonads look like in females with Turner's Syndrome?
|
90% have streak gonads, 10% have ovaries
|
|
A person with chromosomes (XXY) are said to have....?
|
Klinefelter's Syndrome
|
|
People with chromosomes (XYY) are said to have......?
|
Uh, (47,XYY) Syndrome
|
|
What are the classical signs of Klinefelter's Syndrome?
|
tall, long limbs, gynecomastia, possible learning disorders
|
|
What are the classical signs of XYY syndrome?
|
nothing, really, they are mostly indistinguishable
|
|
What is the prevalence of babies born with Klinefelter's Syndrome?
|
1/800 live male births
|
|
What is the most common genetic abnormality found in miscarried fetuses?
|
Turner's Syndrome
|
|
What is the prevalence of babies born with Turner's Syndrome?
|
1/3500 live female births
|
|
How many males actually have chromosomes other than (XY)?
|
1 in 400
|
|
How many females actually have chromosomes other than (XX)?
|
1 in 700
|
|
How often are females born with XXX genotype?
|
1 in 1000
|
|
What are the signs of a person with the XXX genotype?
|
Physical abnormalities are minimal, may have menstrual irregularity/infertility
|
|
As the number of extra X chromosomes goes up, what also goes up?
|
Risk for mental retardation
|
|
What is the most common cause of genital ambiguity at birth?
|
Congenital Adrenal Hyperplasia
|
|
What is the most common form of Congenital Adrenal Hyperplasia?
|
the one where you are deficient in 21 hydroxylase
|
|
What is the inheritance pattern for Congenital Adrenal Hyperplasia?
|
autosomal recessive
|
|
What else may you find in babies with 21-OHase deficient Cong. Adrenal Hyperplasia besides ambiguous genitalia?
|
hyponatremia, hyperkalemia, acidosis, hypovolemia, shock
|
|
What else may you find in an 11-OHase deficient Cong. Adrenal Hyperplasia baby besides ambiguous genitalia?
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hypertension, hypokalemia, alkalosis, reduced renin/aldosterone
|
|
Which adrenal deficiencies produce pseudohermaphroditism in females?
|
21-OHase, 11-OHase
|
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Which adrenal deficiencies produce pseudohermaphroditism in males?
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17-OHase, 3-beta hydroxysteroid
|
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What else may you find in a 17-OHase deficient baby boy besides feminine external genitalia?
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hypertension, hypernatremia, hypokalemia
|
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Girls with Cong. Adrenal Hyperplasia are more likely to prefer "boy" activities and excel at spatial reasoning. T/F?
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True. The brain is also masculinized by the excess androgens
|
|
What is the definition of true hermaphroditism?
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posessing both male and female sexual anatomy: ie, one testis and one ovary, or a penis AND a vagina
|
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What is the definition of pseudohermaphroditism?
|
if ovaries, then male external genitalia. If testes, then female external genitalia. No mixing of ovaries and testes
|
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People with Androgen Insensitivity Syndrome have what genotype and what phenotype?
|
genotype is XY, phenotype is female
|
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What happens to the gonads in people with Androgen Insensitivity Syndrome?
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they turn into testes, but are undescended
|
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What external and internal genitalia do people with AIS have?
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external genitalia is normal female, internal female genitalia is absent; no uterus, fallopian tube, vagina ends in blind pouch
|
|
What is the gender identity of people with AIS?
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Female. There is no masculinization of the brain
|
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What is the phenotype and genotype of people with 5-alpha-reductase syndrome (guevodoces)?
|
XY genotype. Female phenotype as a child, male phenotype at puberty and adulthood
|
|
What is the internal genitalia of people with 5-alpha-reductase syndrome?
|
male. All the internal male parts are intact
|
|
What is the external genitalia of people with 5-alpha-reductase syndrome?
|
female or feminized at birth, may have a shallow, blind vagina. Masculinize at puberty
|
|
What gender identity do people with 5-alpha-reductase syndrome have?
|
in the end, it's usually male, due to testosterone influence on the brain during fetal growth and then at puberty
|
|
What is the definition of true hermaphroditism?
|
posessing both male and female sexual anatomy: ie, one testis and one ovary, or a penis AND a vagina
|
|
What is the definition of pseudohermaphroditism?
|
if ovaries, then male external genitalia. If testes, then female external genitalia. No mixing of ovaries and testes
|
|
People with Androgen Insensitivity Syndrome have what genotype and what phenotype?
|
genotype is XY, phenotype is female
|
|
What happens to the gonads in people with Androgen Insensitivity Syndrome?
|
they turn into testes, but are undescended
|
|
What external and internal genitalia do people with AIS have?
|
external genitalia is normal female, internal female genitalia is absent; no uterus, fallopian tube, vagina ends in blind pouch
|
|
Which cells secrete anti-mullerian hormone?
|
Sertoli cells
|
|
How does the secretion of GnRH affect sex hormone release?
|
pulsatile release of GnRH stimulates sex hormone release. Steady release of GnRH inhibits sex hormone release
|
|
What is the half-life of LH and FSH in the plasma?
|
about 1 hour
|
|
Which gonadal cells respond primarily to LH?
|
Leydig and Thecal cells
|
|
Which gonadal cells respond primarily to FSH?
|
Sertoli and Granulosa cells
|
|
What does LH stimulate in interstitial gonadal cells?
|
sex steroid production
|
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What does FSH stimulate in supporting interstitial gonadal cells?
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aromatase expression, maturation of gametes
|
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A single cell doesn't make both testosterone AND estrogen except for cells of the.....?
|
Corpus Luteum
|
|
Sertoli cells also make ABP. What does it do?
|
Binds testosterone in the cytoplasm, to keep it around for awhile
|
|
Sertoli cells make growth factors that stimulate the proliferation of......?
|
Leydig cells
|
|
What is the quaternary structure of inhibin?
|
one alpha and one betaA chain, or one alpha and one betaB chain
|
|
What does inhibin do?
|
Inhibins FSH release. Does not affect LH or hypothalamus
|
|
What kind of inhibin do the testes make?
|
Type B (one alpha and one betaB chain)
|
|
What kind of inhibin do the ovaries make?
|
both type A and B
|
|
How are the structures of inhibin and activin similar?
|
both are dimers, inhibin of one alpha and one beta; activin of 2 betas
|
|
What does activin do in the gonad?
|
Nobody knows
|
|
What is the quaternary structure of activin?
|
2 betaA chains, or 2 betaB chains, or one betaA and one betaB
|
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What pituitary hormone inhibits GnRH release?
|
prolactin
|
|
What is estrogen's effect on prolactin?
|
estrogen stimulates prolactin release
|
|
What happens to levels of FSH and LH if gonad function is compromised?
|
it goes up, because you lose the inhibitory effect of the sex steroids
|
|
In boys, at what age is puberty typically finished?
|
16 years old
|
|
In girls, at what age is puberty typically finished?
|
14 years old
|
|
What are the symptoms of Kallmann's Syndrome?
|
anosmia (no sense of smell), failure of pubertal development
|
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Where do GnRH secreting neurons come from in the developing fetus?
|
the olfactory epithelium
|
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What is the pathology behind the symptoms seen in Kallmann's Syndrome?
|
both olfactory neurons and GnRH secreting neurons come from the same source: fetal olfactory epithelium
|
|
A woman has uterine leiomyomas. How do you treat her?
|
With a steady does of GnRH to inhibit estrogen release
|
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A man suffers from prostatic hyperplasia. How do you treat him?
|
With a steady does of GnRH to inhibit testosterone release
|
|
How many germ cells does one Sertoli cell touch?
|
about 47
|
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How many other sertoli cells does one sertoli cell make tight junctions with?
|
about 5
|
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What happens in Sertoli-Only Syndrome?
|
germ cells did not migrate to testes. Normal hormones, normal testis structure, but no sperm
|
|
What syndrome accounts for 5-10% of all male infertility?
|
Sertoli-Only Syndrome
|
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What sort of receptor does LH activate on the surface of Leydig cells?
|
G-protein coupled receptor
|
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What type of cell produces Sterol-Carrier Protein (SCP) and Sterol-Activating Protein (SAP)?
|
Leydig cells
|
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What sort of receptor does FSH bind to on the surface of Sertoli cells?
|
G-protein coupled receptor
|
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What type of cell produces Androgen-Binding Protein (ABP)?
|
Sertoli cells
|
|
What percent of total serum testosterone is carried bound to a protein?
|
98%. Only 2% is free
|
|
What receptor does testosterone and DHT bind to?
|
The AR (androgen receptor)
|
|
Which tissues respond more to testosterone than DHT?
|
muscle, reproductive organs
|
|
Which tissues respond more to DHT than testosterone?
|
external genitalia, hair follicles, sebaceous glands
|
|
Where are estrogen receptors located in the male?
|
brain, adipose tissue, bone
|
|
In what part of the cell is the androgen receptor located?
|
In the cytoplasm
|
|
What is testosterone's effect on RBC's?
|
Increases their number. That's why males have higher hematocrit that females
|
|
Where are the 3 peaks of testosterone in a male's life?
|
Once in utero (initial differentiation), once in the first year of life (brain masculinization?), one long peak starting at puberty
|
|
Compare post-pubertal males and females in terms of muscle mass, lean body mass, muscle cell number, and body fat
|
due to T, males have:
150% of female muscle mass 150% of female lean body mass 200% of female muscle cell # 50% of female body fat |
|
What is GH and IGF-1 's effect on gonadal function?
|
GH and IFG-1 increase gonadal function
|
|
What is testosterone's effect on GH?
|
testosterone increases GH
|
|
What is testosterone's effect on bone growth?
|
T (and estrogen) causes bone ossification, promotes closure of the epiphyses
|
|
What is GH's effect on bone growth?
|
GH causes balanced cartilage growth and ossification
|
|
Why do people with delayed puberty have longer bones than other people?
|
GH had more time to make the bones grow before testosterone came and ossified them
|
|
What are the 3 stages of spermatogenesis?
|
1) proliferative
2) meiotic 3) spermiogenic |
|
What happens during the proliferative phase of spermatogeneis?
|
the spermatogonia produce spermatocytes, and maintain their number by self-renewal
|
|
What are the 3 types of spermatogonia, from least differentiated to most differentiated?
|
Type Adark, Type Apale, TypeB
|
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Which subtype of spermatogonia does the spermatocyte directly come from?
|
Type B
|
|
What happens during the meiotic phase of spermagogenesis?
|
1 spermatocyte undergoes meiosis, producing 4 spermatids
|
|
How many chromosomes does a spermatogonia have?
|
46, 2n, diploid
|
|
What happens during the spermiogenesis phase of spermatogenesis?
|
haploid spermatids mature into their final state
|
|
What are the 4 stages of spermiogenesis ? (which itself is the last phase of spermatogeneis)
|
1)golgi phase
2)cap phase 3)acrosomal phase 4)maturation phase |
|
What happens during the golgi phase of spermiogenesis?
|
golgi synthesis the acrosome
|
|
What happens during the cap phase of spermiogenesis?
|
acrosome moves to one pole of the nucleus, and centrioles move to the other pole
|
|
What happens during acrosomal phase of spermiogenesis?
|
Acrosome reaches its final position, centrioles, synthesize the sperm tail, cytoplasm is sloughed
|
|
What happens during the maturation phase of spermiogenesis?
|
sperm leave the teste, move to epididymus, and become capable of fertilization
|
|
What are the 3 parts of the epididymus?
|
head, body, and tail
|
|
Wat happens to sperm in each of the three parts of the epididymus?
|
head: sperm are concentrated
body: sperm aquire movement tail: sperm are stored for release |
|
70% of sperm in the male reproductive tract are stored in the.....
|
tail of the epididymus
|
|
How long does the sequence of spermatogenesis take?
|
64 days
|
|
How does your body keep a steady supply of sperm?
|
every 16 days, spermatogonia start the process again
|
|
Which 2 androgens are responsibly for the vast majority of activity in the male?
|
testosterone and DHT
|
|
What is a normal testosterone level in a male?
|
300-1000 ng/dl
|
|
What is a normal testosterone level in a female?
|
15-65 ng/dl
|
|
Where is testosterone made in a female?
|
50% in ovary, 25% in adrenal cortex, 25% extraglandular
|
|
exogenous testosterone is metabolized rapidly by the.....?
|
liver
|
|
Adding an ester to the 17carbon of testosterone does what?
|
makes it more lipid soluable
|
|
Adding an alkyl group to the 17carbon of testosterone does what?
|
makes oral administration more effective
|
|
Why should you avoid giving testosterone orally?
|
Oral testosterone is very hepatotoxic
|
|
What is the most common use of testosterone therapy?
|
hypogonadism
|
|
What 7 disease states do you treat with testosterone therapy?
|
hypogonadism, breast carcinoma, decreased erythropoesis, osteoporosis, endometriosis, hormone replacement in men, muscle wasting in AIDS
|
|
How does testosterone therapy work against breast carcinoma?
|
acts as an anti-estrogen. Doesn't work any better than other drugs, though
|
|
How does testosterone therapy work to increase erythropoeisis?
|
Testosterone increases the rate of erythropoeisis?
|
|
Which methods of testosterone delivery result in steady serum levels?
|
patch, gel, sublingual tab
|
|
What are some disadvantages of testosterone delivery IV?
|
fluctuating serum levels, risk of infection
|
|
What percent of 12th graders reported using anabolic steroids at least once?
|
2%
|
|
What are some side effects of testosterone therapy in women?
|
virilization, facial hair, deeper voice, acne
|
|
What are some side effects of testosterone therapy in men?
|
prolonged erection, decreased sperm count, gynecomastia
|
|
What are some side effects of testosterone therapy seen in both men and women?
|
edema, jaundice, liver damage, elevated LDL, polycythemia, sleep apnea
|
|
What is leuprolide and what is it used for?
|
leuprolide is a GnRH agonist, used in a steady dose to inhibit testosterone production
|
|
What is plenaxis and what is it used for?
|
plenaxis is a GnRH antagonist, used to inhibit testosterone production
|
|
What is finasteride and what is it used for?
|
finasteride inhibits 5alpha-reductase, used to treat testosterone-overproduction
|
|
What is cyproterone acetate, and what is it used for?
|
cyproterone acetate is a steroid that blocks the AR receptor, used to treat testosterone excess
|
|
What are some side effects of testosterone therapy seen in both men and women?
|
edema, jaundice, liver damage, elevated LDL, polycythemia, sleep apnea
|
|
What is leuprolide and what is it used for?
|
leuprolide is a GnRH agonist, used in a steady dose to inhibit testosterone production
|
|
What is plenaxis and what is it used for?
|
plenaxis is a GnRH antagonist, used to inhibit testosterone production
|
|
What is finasteride and what is it used for?
|
finasteride inhibits 5alpha-reductase, used to treat testosterone-overproduction
|
|
What is cyproterone acetate, and what is it used for?
|
cyproterone acetate is a steroid that blocks the AR receptor, used to treat testosterone excess
|
|
What is flutamide, and what is it used for?
|
flutamide is an androgen receptor blocker, used to treat testosterone excess. It is not a steroid
|
|
What percent of cryptorchid cases have only one undescended testicle?
|
75%
|
|
What is the greatest health risk of cryptorchidism?
|
testicular cancer
|
|
How many times more likely is an undescended tesicle to develop cancer than a normal testicle?
|
cryptorchid testis is 10-40 fold more likely to develop cancer than a normal testicle
|
|
(t/f) in unilateral cryptorchidism, the descended tesicle is not at increased risk for cancer.
|
False! both testes are at risk for cancer in cryptorchidism
|
|
What is the most common cause of tesicular atrophy in the USA?
|
athersclerosis
|
|
What is the most common cause of atrophied testes worldwide?
|
malnutrition
|
|
Why are the testes atrophied in Klinefelter's syndrome?
|
tubular scarring, no elastic fibers, leydig cell hyperplasia
|
|
How does Immotile Cilia Syndrome make a guy infertile?
|
sperm can't move
|
|
What are the acquired 4 ways in which a testis can be rendered infertile?
|
1) torsion
2) varicocele 3) obstruction 4) inflammation |
|
What are FSH/LH and T levels in a man with Klinefelter's Syndrome?
|
high FSH/LH, low T
|
|
What are the 5 common inflammatory diseases of the testes?
|
1) nonspecific epididymitis/orchitis
2) Mumps orchitis 3) Tuberculosis Orchitis 4) Syphilis 5) Granulomatous/autoimmune |
|
What is the most common cause of non-specific epididymitis/orchitis in adults?
|
STDs: chlamydia and gonorrhoeae
|
|
What is the most common cause of non-specific epididymitis/orchitis in children?
|
UTI's with gram negative rods
|
|
What is the most common cause of non-specific epididymitis/orchitis in the elderly?
|
enterobacteria
|
|
In non-specific epididymitis/orchitis, in what order are what structures affected?
|
vas deferens/lymphatics first, then epididymus, then testis is last
|
|
In what percent of adult males does mumps continue to mumps orchitis?
|
30%
|
|
What structure is affected before the testes in mumps orchitis?
|
the parotid gland in the face
|
|
Describe the infiltrate in mumps orchitis
|
lympocytic with edema, neutrophils may be present
|
|
Does mumps orchidis result in infertility?
|
Not often.
|
|
Tuberculus orchitis usually manifests in isolation with no other symptoms. True or false?
|
False. Tuberculus orchitis is usually part of systemic tuberculosis disease
|
|
what will you see on histology if you look at a nut suffering from tuberculus orchitis?
|
caseating granulomas
|
|
where does tuberculus orchitis start?
|
starts in the epididymus, then moves to the testis
|
|
where does syphilis orchitis start?
|
starts in the testes, then moves into the epididymus
|
|
Decsribe the infiltrate seen in syphilis orchitis
|
diffuse lymphocytic, less edema, rich in plasma cells
|
|
Which inflamamtory testicular disease process results in obliterative endarteritis?
|
syphilis orchitis
|
|
What is a gumma, and where would you find one?
|
a necrotized ball of tissue/inflammatory infiltrate, found in the testes during syphilis
|
|
What is the most common type of testicular cancer?
|
Germ cell cancer, 95%
|
|
What demographic do germ cell cancers tend to affect?
|
young men, 15-35 years old
|
|
How does a germ cell tumor manifest?
|
painless testicular enlargement
|
|
What are the 6 types of germ cell tumor?
|
1) seminoma
2) spermatocytic seminoma 3) embryonal carcinoma 4) yolk sac tumor 5) choriocarcinoma 6) teratoma |
|
What is the most common type of germ cell tumor?
|
seminoma
|
|
Which type of germ cell tumor can result in syncytiotrophoblastic giant cells that secrete ________?
|
seminomas can have those kinds of cells, which secrete hCG
|
|
What do seminomas look like grossly?
|
fish flesh, whatever that means
|
|
What do seminomas look like on histology?
|
uniform, polygonal cells, clear cytoplasm, prominent nucleolus
|
|
Which type of germ cell tumor affects older men more than younger ones?
|
spermatocytic seminoma
|
|
What does a spermatocytic seminoma look like on histology?
|
like primary and secondary spermatocytes
|
|
What is the most malignant type of germ cell tumor?
|
embryonic carcinoma
|
|
What do embryonic carcinoma tumors look like on histology?
|
dark, big nuclei, with indistinct cytoplasm
|
|
What is the most common germ cell tumor in children?
|
yolk sac tumor
|
|
What protein do yolk-sac tumors secrete?
|
alpha-fetoprotein
|
|
What do yolk-sac tumors look like on histology?
|
thin sheets of cells around nets of capillaries
|
|
What substance does a choriocarcinoma secrete?
|
hCG
|
|
What is the rarest type of germ cell tumor?
|
choriocarcinoma
|
|
Which extra-embryonal tissue are the germ cells producing in a choriocarcinoma?
|
placenta
|
|
Speaking of germ cell tumors, what does a teratoma look like grossly?
|
loose combination of anything: nerves, muscle, bone ,cartilage, epithelia
|
|
What percent of people with germ cell tumors have more than one kind?
|
60%
|
|
Other than germ cell tumors, what are the other two types of testicular cancers?
|
lymphomas, and sex cord stroma tumors
|
|
what are the two types of sex-cord-stroma tumors, and which is more common?
|
leydig cell tumor (2% of testicular tumors) and sertoli cell tumors (very uncommon)
|
|
What symptoms can a leydig cell tumor cause?
|
gynecomastia and precocious puberty, if it is secreting hormones
|
|
What is a condyloma acuminatum?
|
a genital wart on the penis
|
|
What can cause a condyloma acuminatum?
|
human papilloma virus
|
|
What does a koilocyte look like, and in what cases would you see one?
|
koilocytes are seen in Human Papilloma virus infection, and have crinkly nuclei and large perinuclear halo
|
|
What is a verrucous carcinoma, and where would you see one?
|
a giant genital wart, right there on the penis.
|
|
Bowen's Disease is:
|
squamous cancer in situ of the skin in the genital region
|
|
Squamous cancer in situ on the skin in the genital region is called?
|
Bowen's Disease
|
|
Squamous cancer in situ on the mucosa of the penis is called?
|
Queyrat's Disease
|
|
Queyrat's Disease is?
|
squamous carcinoma in situ of the mucosa of the penis
|
|
Which subtypes of HPV are implicated in squamous carcinoma of the male genitals?
|
16 and 18
|
|
african american:caucasian ratio of squamous carcinoma in situ of the penis
|
2:1
|
|
Where and what is the verumontanum?
|
In the prostate, where the ejaculatory duct meets the urethra at a 35 degree angle
|
|
What hormone stimulates the prostate to do its thing?
|
DHT
|
|
What are the 3 zones of the prostate?
|
central, transitional, peripheral
|
|
where is the central zone in the prostate?
|
surrounds the ejaculatory duct
|
|
where is the transitional zone in the prostate?
|
surrounds the proximal urethra, before the verumontanum
|
|
where is the peripheral zone?
|
surrounds the distal urethra, after the verumontanum
|
|
When does the prostate start to develop "prostate sand," and what is it?
|
as you grow older, prostatic secretions precipitate out and form solid deposits
|
|
What are the 5 common pathological categories of prostatic dysfunction?
|
1) inflammation
2) BPH 3) adenocarcinoma 4) PIN 5) other malignancies |
|
What is the histological difference between acute and chronic prostatitis?
|
acute: neutrophils present
chronic: lymphocytes present |
|
What are the most common causes of acute prostatitis?
|
E coli and S aureus from bladder infections
|
|
What is malakoplakia, and what organ does it affect?
|
calcified bacterial remnants (Michaelis-Gutmann bodies) lodged in the prostate
|
|
What are symptoms common to all inflammatory prostatic diseases?
|
obstructive urinary symptoms, low back pain, dysuria
|
|
In which zone of the prostate does BPH manifest?
|
transitional zone
|
|
what is the prevalence of BPH?
|
starting at 50, the law of tens: 50% of men 50 years old, 70% of men 70 years old, etc
|
|
What is the most common way to treat symptomatic BPH?
|
anti-androgens and alpha blockers
|
|
What percent of men with BPH need surgery?
|
5-10%
|
|
What are the symptoms of BPH?
|
nocturia, difficulty in starting/stopping urine flow, frequent urination
|
|
BPH can involve 3 prostatic tissues in various amounts:
|
epithelia, stroma, and smooth muscle
|
|
In men, how common is prostate adenocarcinoma?
|
2nd most common cancer after skin cancer
|
|
What factors predispose to prostate adenocarcinoma?
|
age (over 50), race (blacks > whites >>>> orientals), diet, family history
|
|
what are the clinical signs of prostatic adenocarcinoma?
|
asymptomatic, or sometimes similar to BPH
|
|
What zone of the prostate is most commonly affected by adenocarcinoma?
|
peripheral zone
|
|
What do prostate adenocarcinoma tumors look like, grossly?
|
yellowish, or unapparent
|
|
what do prostate adenocarcinoma tumors look like, microscopically?
|
atypical glands lined by single layer of malignant columnar cells with prominent nucleoli
|
|
What is the Gleason grade used for?
|
to grade prostate cancer outcomes
|
|
What is the Gleason Grade based on?
|
gland patterns in the prostate. The more abberant, the higher the grade.
|
|
Where do prostate adenocarcinomas commonly metastasize to?
|
axial skeleton, lymph nodes
|
|
Local prostate adenocarcinoma, confined to the prostate capsule, is treated how?
|
prostatectomy, beam radiation, radioactive "seeds"
|
|
Advanced prostate adenocarcinoma, beyond the prostate capsule, is treated how?
|
androgen ablation therapy, like orchiectomy, anti-androgen pills, alpha-reductase inhibitors, etc.
|
|
What hormones do prostate adenocarcinoma tumors grow in response to?
|
androgens
|
|
What substance is used as a clinical marker of prostate cancer?
|
Prostate-specific antigen (PSA), and occasionally alk phos
|
|
What is the gold standard for diagnosis of prostate adenocarcinoma?
|
fine needle biopsy
|
|
Malignancies of the prostate other than adenocarcinoma include:
|
sarcoma, lymphoma, neuroendocrine-oid tumors
|
|
Which are more aggressive: prostatic adenocarcinomas or other prostatic malignancies?
|
The other malignancies (sarcoma, lymphoma, etc)
|
|
What is PIN?
|
Prostatic Intraepithelial Neoplasia
|
|
What do PINs look like on histology?
|
tufted knobs of cells growing into the prostatic gland lumen, covered by basal cell layer
|
|
What does PIN lead to?
|
adenocarcinoma
|
|
Quick review! what are the 3 layers of the adrenal cortex and what do they secrete?
|
glomerulosa - aldosterone
fasciculata - cortisol reticulata - androgens |
|
What does Steroid Acute Regulatory Protein (StAR) do?
|
moves cholesterol into the mitochondria of adrenal cortex cells
|
|
What enzyme converts cholesterol into pregnenolone?
|
20-22 desmolase
|
|
If you have no StAR protein, what happens to the adrenal cortex?
|
fills with cholesterol and secretes NOTHING
|
|
In general, what is the ACTH level in a person with CAH?
|
very high
|
|
Deficiency of what enzyme is the most common cause of CAH?
|
21-OHase
|
|
People with the 21-OHase deficient form of CAH have a buildup of what substance?
|
17-OH progesterone
|
|
What would the relative levels of sodium and potassium be in people with 21-OHase deficient CAH?
|
Low salt and high potassium
|
|
How does 21-OHase deficient CAH manifest in females?
|
Females are virilized
|
|
How does 21-OHase deficient CAH manifest in males?
|
May not show up until they have delated puberty
|
|
What is the second most common form of CAH?
|
11-OHase deficiency (>5%)
|
|
What are the relative sodium and potassium levels in a person with 11-OHase deficient CAH?
|
high sodium, low potassium
|
|
Why do people with 11-OHase deficient CAH retain salt?
|
No aldosterone, but a buildup of 11-deoxycorticosterone, which is similar
|
|
How does 11-OHase deficient CAH manifest in females?
|
Virilized at birth
|
|
How does 11-OHase deficient CAH manifest in males?
|
may not show up until delayed puberty
|
|
How does 3-beta hydroxysteroid deficient CAH manifest itself in females?
|
might not be found until delayed adrenarche in puberty
|
|
How does 3-beta hydroxysteroid CAH manifest itself in males?
|
males are born with ambiguous genitalia
|
|
What are the relative levels of sodium and potassium in a person with 3-beta hydroxysteroid deficient CAH?
|
low sodium, high potassium
|
|
How does 17-OHase deficient CAH manifest itself in females?
|
might not be found until delayed adrenarche in puberty
|
|
How does 17-OHase deficient CAH manifest itself in males?
|
Males are born with ambiguous genitalia
|
|
What are the relative levels of sodium and potassium in a person with 17-OHase deficient CAH?
|
high sodium, low potassium
|
|
What does ketoconazole do to testosterone synthesis?
|
It shuts it down
|
|
Define gonadarche
|
The re-emergence of the hypo-pit-gonad axis during puberty
|
|
Define adrenarche
|
production of adrenal androgens, which is NOT under the control of the hypo or pituitary
|
|
What is the first sign of puberty in a boy?
|
testicular enlargement greater than 3 cc
|
|
What is the first sign of puberty in a girl?
|
breast bud development
|
|
Normal onset of puberty in boys is
|
9-14 years old
|
|
Normal onset of puberty in girls is
|
8-13 years old
|
|
What is the average age of menarche in caucasian girls?
|
12.5 years old
|
|
puberty in black/hispanic girls starts when, in relation to white girls?
|
1 year earlier
|
|
What constitutes Delayed Puberty in boys?
|
No testicular enlargement by 14 years old
|
|
What constitutes Delayed Puberty in girls?
|
No breast development by 13 years old,
OR no menses 4 years after pubertal onset, OR no menses by 16 years old |
|
What are the relative FSH and LH levels in a pre-pubertal kid?
|
FSH is higher than LH
|
|
What are the relative FSH and LH levels in a pubertal or post-pubertal kid?
|
LH is higher than FSH
|
|
High gonadotropins in a kid with delayed puberty suggest a defect in....?
|
the gonad itself
|
|
Low gonadotropin levels in a kid with delayed puberty suggest the problem is.....?
|
with the hypothalamus or pituitary
|
|
What is the most common cause of delayed puberty?
|
constitutional delay
|
|
What is the bone-age of kids with constitutional delay?
|
appropriate for whatever stage of puberty they are in (or not in)
|
|
What is the pathology of constitutional delay?
|
There is none. Puberty progesses normally, just starts later
|
|
What outside factors may contribute to suppressed gonadotropin levels in hypogonadotropic hydogonadism?
|
illness, stress, excessive exercise, malnutrition, anorexia
|
|
What endocrine factors can cause low FSH/LH levels in people with hypogonadotropic hypogonadism?
|
hyperprolactinemia, hypothyroidism, isolated gonadotropin deficiency, hypopituitarism
|
|
What congenital factors can cause low FSH/LH levels in people with hypogonadotropic hypogonadism?
|
Kallmann Syndrome, Prader-Willi Syndrome, CNS defects
|
|
What acquired factors can cause low FSH/LH levels in people with hypgonadotropic hypogonadism?
|
trauma, irradiation, infection, autoimmunity
|
|
What congenital factors can cause high FSH/LH levels in people with hypergonadotropic hypogonadism?
|
Klinefelter's, Turner's, gonadal dysgenesis, Noonan syndrome
|
|
What acquired factors can cause high FSH/LH levels in people with hypergonadotropic hypogonadism?
|
chemotherapy, irradiation to the pelvis, torsion/trauma, orchitis, cryptorchism
|
|
What tests should be run in a kid with delated puberty?
|
Bone age, body measurements, FSH/LH levels, prolactin, thyroid, Testosterone and estrogen, blood count, ESR
|
|
At what age does puberty start in a boy with precocious puberty?
|
under 9 years old
|
|
At what age does puberty start in a caucasian girl with precocious puberty?
|
under 8 years old
|
|
At what age does puberty start in a black/hispanic girl with precocious puberty?
|
under 7 years old
|
|
Which form of precocious puberty is identical to normal puberty, but it just starts sooner?
|
central (gonadotropin-dependant) precocious puberty
|
|
What is the most common cause of precocious puberty in boys?
|
CNS lesion
|
|
What 4 things can result in bilateral testicular enlargement in pre-pubertal boys?
|
1) central precocious puberty?
2) LH receptor activation by a hCG producing tumor 3) testitoxicosis 4) McCune-Albright Syndrome |
|
What is usually the cause of unilateral testicular enlargement?
|
testicular tumor
|
|
What test distinguishes between central and peripheral precocious puberty?
|
GnRH stimulation test
|
|
How will a patient with central precocious puberty respond to the GnRH stimulation test?
|
Their response will be pubertal, with LH > FSH
|
|
How will a patient with peripheral precocious puberty respond to the GnRH stimulus test?
|
They will produce pre-pubertal levels: FSH > LH
|
|
What is the treatment for central precocious puberty?
|
Leuprolide
|
|
Peripheral precocious puberty due to McCune Albright Syndrome in girls is treated with:
|
aromatase inhibitors
|
|
Peripheral precocious puberty due to McCune Albright Syndrome in boys is treated with:
|
ketoconazole, or androgen blockers/aromatase inhibitors
|
|
Peripheral precocious puberty due to familial testitoxicosis in boys is treated with:
|
ketoconazole, or androgen blockers/aromatase inhibitors
|
|
benign premature adrenarche is characterized by what symptoms?
|
body hair growth in pre-pubertal kids, with no growth or bone age advancement
|
|
What characterizes benign premature thelarche?
|
breast development with no other signs of puberty, growth, or bone age advancement. Usually seen in girls under 2 years old.
|
|
Acquired hypogonadotrophic hypogonadism in males can be due to 4 things:
|
hemochromotosis, pituitary tumors, stress, sleep apnea
|
|
What is the most common pituitary tumor that can cause hypogonadotropic hypogonadism?
|
prolactinoma
|
|
What are the serum levels of LH, FSH, and testosterone in males with hypogonadotrophic hypogonadism?
|
low LH
low FSH low testosterone |
|
lab values for LH, FSH, and testosterone in a boy with Klinefelter's Syndrome:
|
normal LH
low FSH low testosterone |
|
What are the 5 causes of HYPERgonadotropic hypogonadism?
|
1) congenital (anorchia)
2) Klinefelter's Syndrome 3) mutations in androgen receptor 4) acquired (trauma, poison) 5) tumor that makes defective FSH/LH |
|
Lab values for FSH, LH, and testosterone in boys with androgen receptor mutations:
|
high FSH, high LH, high testosterone, but no clinical effects of the androgens
|
|
Lab values for FSH, LH, and testosterone in boys with acquired hypergonadotrophic hypogonadism:
|
high FSH (early)
high LH (late) low testosterone |
|
What are some ways for boys to get Acquired Hypergonadotrophic Hypogonadism?
|
torsion, mumps, orchitis, alcohol, chemotherapy, diabetes
|
|
Lab values for FSH, LH, and testosterone in boys with a tumor that secretes mutated FSH and LH:
|
high FSH
high LH low testosterone (the FSH/LH react with the assay, but have no biologic activity |
|
What is the treatment for hypergonadotrophic hypogonadism in men?
|
androgens, GnRH, hCG
|
|
What groups of men are contraindicated for androgen therapy who suffer from hypergonadotrophic hypogonadism?
|
those with hormone-sensitive cancers (prostate cancer)
|
|
How many oogonia are in the ovaries of a female fetus at 20 weeks gestation?
|
6-7 million
|
|
At birth, how many oogonia does a female baby have?
|
1-2 million
|
|
At puberty, how many oogonia does a female have?
|
400,000
|
|
Each menstrual cycle, about how many oogonia compete for the privilege of being released?
|
10-30
|
|
When in a female's life do her oogonia start meiosis 1?
|
as a fetus
|
|
Primary oocytes are frozen in what stage of the cell cycle?
|
prophase of meiosis 1
|
|
What is the state of the chromosomes in a primary oocyte?
|
diploid chromosomes (46), each of which is duplicated (4N)
|
|
What prompts a primary oocyte to move forward out of prophase 1?
|
The LH surge of the menstrual cycle
|
|
The LH surge prompts the primary oocyte to do......what now?
|
complete meiosis 1, and form the secondary oocyte and the first polar body
|
|
What is the state of the chromosomes in a secondary oocyte?
|
haploid chromosomes (23), duplicated DNA (2N)
|
|
How is the secondary oocyte different from the first polar body? How is it the same?
|
secondary oocyte: larger, more cytoplasm
polar body: tiny tiny. both are duplicated haploid (23, 2N) |
|
At what stage of the cell cycle is the secondary oocyte frozen at?
|
Meiosis 2
|
|
When does the secondary oocyte complete meiosis 2?
|
at fertilization
|
|
Where does the second polar body come from?
|
when the secondary oocyte completes meiosis 2, forming the bigger egg and the smaller 2nd polar body
|
|
Is there a genetic difference between polar body 1 and polar body 2?
|
yes.
polar body 1: duplicated haploid (23, 2N) polar body 2: single haploid (23, 1N) |
|
Which phase of the menstrual cycle, in terms of ovarian function, is the most consistant in its duration?
|
The luteal phase
|
|
Name the stages of follicular development in order:
|
primordial follicle -> primary follicle -> secondary follicle -> tertiary follicle -> graafian follicle
|
|
Pre-antral follicles include which stages?
|
primordial, primary, and secondary follicles
|
|
Antral follicles include which stages?
|
tertiary and graafian
|
|
After the egg is released, the follicle turns into the _________, which then turns into the ____________.
|
corpus luteum, corpus albicans
|
|
What distinguishes the dominant follicle from the rest of the follicles in the cohort?
|
the dominant follicle has a better blood supply, more estrogen around it, more FSH receptors
|
|
what are the layers found in a cross-section of a primordial follicle, from the center to the outside
|
primary oocyte, pregranulosa cells, basement membrane
|
|
What is the zona pelludida made of?
|
glycoproteins excreted from both the primary oocyte and the granulosa cells
|
|
What is the purpose of the zona pellucida?
|
lets only one sperm into the egg, blocks off all the others
|
|
what are the layers found in a cross-section of a primary follicle, from the center to the outside?
|
primary oocyte, zona pellucida, granulosa cells, basement membrane
|
|
what are the layers of a cross-section of a secondary follicle, from the inside to the outside?
|
primary oocyte, zona pellucida, several layers of granulosa cells, basement membrane, theca cells
|
|
At what stage of the follicle's development do the granulosa and theca cells express FSH and LH receptors, thereby becoming hormonally active?
|
when they become secondary follicles
|
|
What are the layers of a cross-section of a tertiary follicle, from the inside to the outside?
|
primary oocyte, zona pellucida, granulosa cells, antrum, granulosa cells, basement membrane, theca interna, theca externa
|
|
Inside a follicle, what is the antrum?
|
fluid filled space that separates the egg and company from the rest of the follicle
|
|
Inside a follicle, what is the cumulus oophorus?
|
the stalk of cells connecting the egg to the rest of the follicle. dissapears as the antrum completes development
|
|
What is the corona radiata?
|
the group of granulosa cells that is expelled from the ovary along with the egg and zona pellucida
|
|
What are the layers of a cross-section of a graafian follicle, from the inside to the outside?
|
primary or secondary oocyte, zona pellucida, corona radiata, antrum, granulosa cells, basement membrane, theca interna, theca externa
|
|
All the stages of follicular development contain primary oocytes, except for which one?
|
graafain follicles contain either primary or secondary oocytes, depending on whether the LH surge has occured or not
|
|
What does the corpus luteum do, after the oocyte is released?
|
secretes a lot of progesterone and estrogen
|
|
How long does the corpus luteum secrete hormones if the egg implants?
|
about 9 weeks, until the placenta can take over hormone secretion
|
|
how long does the corpus luteum secrete hormones if the egg does NOT implant?
|
about 11 days, and then it stops.
|
|
What is the most apparent effect of the corpus luteum's stoppage of hormone secretion in the case of non-implantation?
|
falling progesterone stimulates the uterus to shed its lining, leading to menstrual flow
|
|
In the case of egg implantation, what keeps the corpus luteum secreting hormones for those 9 weeks?
|
the conceptus secretes hCG, which stimulates the corpus luteum until the placenta takes over
|
|
How does the hypothalamus behave differently during the luteal phase compared with the follicular phase?
|
GnRH pulses are more frequent, but smaller, during follicular phase, as compared with the luteal phase
|
|
When during the menstrual cycle are FSH and LH levels equal?
|
early in the follicular phase
|
|
At the end of the luteal phase, what are the relative levels of FSH and LH?
|
FSH increases 3x, LH increases 2x
|
|
When during the menstrual cycle are FSH and LH levels at their highest?
|
right before ovulation
|
|
What stimulates the LH surge?
|
sustained high levels of estrogen
|
|
The menstrual cycle, in terms of what's going on in the uterus, can be divided into three stages, which are:
|
proliferative phase, secretory phase, menstrual phase
|
|
What are the three levels of the endometrium, from deepest to most superficial?
|
stratum basalis, stratum spongiosum, stratum compactum
|
|
Which layer of the endometrium does not change much during the menstrual cycle?
|
the stratum basalis
|
|
What two types of arteries feed the endometrium? Which layers do they feed?
|
straight arteries stay in the stratum basalis, and spiral arteries go up into the stratum spongiosum/compactum
|
|
What happens to the endometrium of the uterus during the proliferative phase of the menstrual cycle?
|
stroma thickens, gets vascular, glands form and elongate
|
|
What hormone brings about the changes in the endometrium during the proliferative phase of the menstrual cycle?
|
estrogen from the ovaries
|
|
What happens to the endometrium of the uterus during the secretory phase of the menstrual cycle?
|
glands become tortuous and squiggly, and secrete glycogen and fluid
|
|
the changes in the endometrium during the secretory phase of the menstrual cycle are due to what hormone?
|
progesterone from the corpus luteum
|
|
What happens to the endometrium of the uterus during the menstrual phase of the menstrual cycle?
|
spiral arteries necrose, ischemia causes the stratum spongiosum/compactum to degrade and slough off
|
|
What hormonal is responsible for the changes in the endometrium seen during the menstrual phase of the menstrual cycle?
|
falling levels of progesterone and estrogen stimulate the endometrium to be sloughed off
|
|
About how long does the menstrual phase of the menstrual cycle last?
|
5 days
|
|
About how long does the luteal phase of the menstrual cycle last?
|
14 days
|
|
during the follicular phase of the menstrual cycle, how often do you have a GnRH pulse?
|
1 every hour
|
|
during the luteal phase of the menstrual cycle, how often do you have a GnRH pulse?
|
1 every 3-4 hours
|
|
What levels of estrogen do you need to acheive the LH surge?
|
greater than 200 picograms for over 50 hours
|
|
Average amount of blood loss during menses is.......?
|
30 cc
|
|
What is estrogen's effect on cholesterol?
|
estrogen increases HDL, decreases LDL
|
|
What are the 3 main pharmacological uses of estrogen therapy?
|
hypogonadism in women, menopause, and contraception
|
|
What are 6 deletarious side-effects of of taking exogenous estrogen?
|
cardiovascular risks, cancer, changes in lipid metabolism, gall bladder disease, migraines, thromboembolisms, hypertension
|
|
What are SERMs, and what is so great about them?
|
Selective Estrogen Receptor Modulators; these drugs are agonists or antagonists, depending on the tissue, so you can get more good effects with less bad effects
|
|
What are the 5 general targets that exogenous estrogen can target?
|
breast, bone, endometrium, blood vessels, CNS.
|
|
For the best outcomes, SERMs should act as agonists in which tissues?
|
bone, blood vessels, CNS
|
|
For the best outcomes, SERMs should act as antagonists at which tissues?
|
breast, endometrium
|
|
Which SERMs are used to treat breast cancer?
|
tamoxifen, toremifene
|
|
Which SERMs are used to prevent osteoporosis?
|
raloxifene
|
|
What is the biggest risk for a women taking tamoxifen?
|
endometrial cancer
|
|
Who would you give clomiphene to? How does it bring about its therapeutic effects?
|
clomiphene is an anti-estrogen, and treats infertility by increasing GnRH levels by blocking estrogen's negative feedback
|
|
What are some physiologic actions of progesterone in women?
|
negative feedback on GnRH, blocks estrogen-driven endometrial proliferation, stimulates secretory endometrium
|
|
What hormone makes cells more responsive to progesterone?
|
estrogen
|
|
What are some pharmacologic uses of exogenous progesterone?
|
hormone replacement in women, cancer, contraception, dysmenorrhea
|
|
What is mefipristone, and what is it used for?
|
mefipristone is an anti-progesterone, used as a pregnancy terminator and ovulation preventer
|
|
What do you do first when evaluating a women with altered levels of sex hormones?
|
Check hCG levels to see if she's pregnant!
|
|
10% of amenorrheic women suffer from.......?
|
a prolactinoma
|
|
When evaluating women with sex hormone disturbances, check androgen levels only if.......?
|
she is suffering from hirsutism or acne
|
|
A women is amenorrheic, is not pregnant, does not have a prolactinoma. What is the next stage of testing?
|
induce menses with progesterone (5 mg daily for 5 days). 5 days after the bleeding, draw FSH and LH levels, which are equal in normal people
|
|
What are some causes of hypogonadotropic hypogonadism in women?
|
Kallmann's Syndrome, stress, malnutrition, excessive exercise
|
|
What are levels of FSH, LH, and estrogen in women with hypogonadotropic hypogonadism?
|
low LH, low FSH, low estrogen
|
|
What are levels of FSH, LH, and estrogen in women with hypergonadotropic hypogonadism?
|
high FSH, high LH, low estrogen
|
|
What are common causes of hypergonadotropic hypogonadism in females?
|
Turner's Syndrome, Premature Ovarian Failure
|
|
Premature Ovarian Failure is usually due to:
|
autoimmunity
|
|
Lab values for a women with Premature Ovarian Failure for LH, FSH, and estrogen are:
|
high high FSH (because of inhibin loss)
high LH low estrogen |
|
People with PCOS begin to show symptoms..... when?
|
during puberty, ALWAYS. These people have ALWAYS had period problems. It doesn't appear later in life.
|
|
What are the lab values in a women with PCOS for LH, FSH, androgens, progesterone, estrogen?
|
high high high LH, low FSH, high androgens, steady estrogen levels, low progesterone
|
|
What do people think is the etiology behind PCOS?
|
GnRH pulses come too fast
|
|
What are some symptoms of PCOS?
|
irregular menses, hirsutism, insulin resistance, acanthosis nigricans, acne, obesity
|
|
What are some risks and complications of having PCOS?
|
endometrial cancer, diabetes, hypertension, heart disease.
|
|
What will be the difference seen in a women with PCOS as opposed to a women with an androgen-producing tumor?
|
the lady with the tumor will have a history of normal periods, with symptoms only showing up recently. She may also have clitorromegaly and male pattern baldness
|
|
How can you distinguish a lady with PCOS from a lady with Obesity-Induced Anovulation?
|
the lady with O.I.A. will have a history of normal periods, and normal LH/FSH ratio. If she loses weight, her periods come back.
|
|
What is the etiology of disease in a women with obesity-induced anovulation?
|
excess estrogen due to aromatase activity in adipose tissue
|
|
How do you treat female hypogonadism?
|
estrogen replacement, progesterone replacement, clomiphene, GnRH pump
|
|
Cytologically, what is the difference between acute and chronic cervicitis?
|
chronic cervicitis: plasma cells and squamous metaplasia present
acute cervicitis: PMNs present, with or without epithelial erosion |
|
What are some risk factors for acquiring an inflammed cervix?
|
STI's, childbirth, hypo/hyperestrogenism, antibiotics, IUD, change in host immunity
|
|
What are some sequelae of cervicitis?
|
vertical transmission during childbirth, spread to uterus/fallopian tubes, abscess, infertility
|
|
There are two benign tumor-like lesions of the cervix, and they are called:
|
nabothian cysts and endocervical polyps
|
|
What is the etiology behind a nabothian cyst?
|
blocked mucus duct leads to inflammation and cyst formation on the cervix
|
|
What is the etiology of an endocervical polyp?
|
hormonal levels cause endocervical glands to undergo hyperplasia
|
|
How do you treat endocervical polyps?
|
curretage pretty much cures them
|
|
How does a liquid prep of a pap smear specimen compare to a slide prep?
|
liquid preps are more sensitive, but more expensive
|
|
When should a women get her first pap smear?
|
3 years after she starts having sex, or at age 21
|
|
How often should a women under 30 years old get a pap smear?
|
every year
|
|
How often should a women over 30 years old get a pap smear?
|
if 3 consecutive paps are normal, then get a new pap every 2-3 years
|
|
What is the guideline for pap smears for women over 70 years old?
|
If they have been normal for the past 10 years, they can stop screening
|
|
When during the menstrual cycle should you get the pap smear done?
|
mid-cycle, not during menstruation
|
|
Which is more common: adenocarcinoma of the cervix, or squamous carcinoma of the cervix?
|
squamous
|
|
What is the cause of granulomatous endometriosis?
|
TB in the uterus or fallopian tubes
|
|
What is the most common cause of infertility WORLDWIDE?
|
granulomatous endometriosis due to TB
|
|
What are the 3 benign tumor-like lesions found in the uterus?
|
uterine polyp, adenomyosis, leiomyoma
|
|
What is the etiology of a uterine polyp?
|
chromosomal weirdness causes endometrial outgrowth. Treat with hysterectomy or polypectomy
|
|
What are some symptoms of a uterine polyp?
|
irregular or excessive bleeding, abnormal pap due to shedding of glands
|
|
What is going on if a woman has adenomyosis of the uterus?
|
endometrial glands extend into the myometrium, causing uterine enlargement
|
|
What are some symptoms of uterine adenomyosis?
|
can be asymptomatic, but you can also have menorrhagia, dysmenorrhea, pelvic pain
|
|
What is going on in a woman who has a leiomyoma?
|
fibroid swellings of uterine tissue, that grow in response to estrogen
|
|
What is the most common mass found in the uterus (besides a fetus)?
|
leiomyomas
|
|
What are some symptoms of having a leimyoma?
|
pain, bleeding not due to menstruation, impaired fertility
|
|
What are the 4 types of endometrial hyperplasia?
|
simple
complex complex with atypia endometrial intraepithelial neoplasia |
|
Simple hyperplasia of the endometrium is characterized by what?
|
mild alteration, cytic gland crowding, some gland distortion
|
|
Complex hyperplasia of the endometrium is characterized by what?
|
moderately altered hyperplasia of the glands
|
|
What percent of complex hyperplasia of the endometrium turn into malignancies?
|
less than 5%
|
|
Complex hyperplasia of the endometrium with atypia is characterized by what?
|
gland crowding, budding, cellular mitotic activity, high grade hyperplasia
|
|
What percent of complex hyperplasia of the endometrium with atypia turns into carcinoma?
|
25%
|
|
What characterizes Endometrial Intraepithelial Neoplasia (EIN)?
|
monoclonal proliferation, usually because of the loss of the PTEN gene
|
|
What percent of EIN in the endometrium progresses to malignancy?
|
39%
|
|
What are 6 risk factors for developing endometrial carcinoma?
|
obesity, diabetes, hypertension, infertility, unapposed estrogen, atypical complex hyperplasia
|
|
What is the median age of diagnosis for endometrial carcinoma?
|
63 years old
|
|
There are 3 kinds of endometrial carcinoma. they are.......?
|
1) endometroid
2) non-endometrioid 3) clear cell |
|
Who usually gets endometroid uterine cancer, what's the prognosis, and what's the etiology?
|
endometroid cancer is usually in younger women, has a better prognosis, and arises from EIN
|
|
Who usually gets non-endometroid uterine cancer, what's the prognosis, and what does it look like?
|
Older women get the non-endometroid cancer, it has a worse prognosis, and resembles serous ovarian tumors
|
|
What are some characteristics of clear cell carcinoma of the endometrium?
|
worse prognosis, rarest form.
|
|
There are 3 types of endometrial sarcomas. They are.....?
|
leiomyosarcoma, endometrial stromal sarcoma, and malignant mixed mullerian tumors.
|
|
How is a leiomyosarcoma different from a leiomyoma?
|
leiomyosarcomas arise in the myometrium, have different microscopic features, and can spread to other sites
|
|
Which endometrial sarcoma has the worst prognosis?
|
Malignant Mixed Mullerian Tumor
|
|
There are 5 non-neoplastic cysts that can appear in the ovary. They are........?
|
corpus luteum cyst, follicle cyst, PCOS cysts, serous inclusion cyst, endometriosis
|
|
Ovarian cancer accounts for ___% of all cancers in women, but _____% of all cancer deaths in women
|
6%, 50%
|
|
Which two genes can predispose you to getting ovarian cancer (if you are a woman, of course)?
|
BRCA-1 and HNCC
|
|
What demographic of women is at most risk of developing ovarian cancer?
|
nulliparous
|
|
What percent of ovarian tumors are benign?
|
80%
|
|
Ovarian neoplasms are divided into 3 broad categories, which are.......? Oh, and which ones are most common?
|
Epithelial (75%)
Germ cell (20%) Sex cord stromal (5%) |
|
Epithelial cancers of the ovary can be lumped into two categories, ______ and ______.
|
serous, mucinous
|
|
What are some characteristics of serous ovarian carcinomas?
|
usually bilateral, contain psamomma bodies
|
|
What are some characteristics of Mucinous Ovarian Carcinomas?
|
cauliflower-like, papillary looking tissue, secrete mucous, usually unilateral
|
|
Ovarian tumors that arise from germ cells come in 4 flavors:
|
dysgerminoma, yolk sac tumor, choriocarcinoma, teratoma
|
|
What are some characteristics of dysgerminomas of the ovary?
|
all maligant, 1/3 are aggressive, very radiosensitive, similar to seminoma in men
|
|
What determines whether a teratoma found in the ovary is likely bengin or likely malignant?
|
teratomas containing undifferentiated tissue (immature) are malignant. Those containing distinct tissue (teeth, hair, skin) are benign
|
|
Sex cord stromal tumors in the ovary usually make themselves known because.....?
|
the tumor secretes hormones which have global effects
|
|
Which is more common to find in the ovary: metastases or primary tumors?
|
metastasies, by a long shot
|
|
Which cancers really like to metastasize to the ovary?
|
colon, fallopian tube, uterus, melanoma, lymphoma, stomach
|
|
Stomach cancer that metastasizes to the ovary has a special name and distictive cytology.......discuss.
|
Krukenberg's Tumor, and on cytology you will see signet ring cells
|
|
Of all the pregnancies in the United States, how many are unintended?
|
50%
|
|
What percentage of people at these ages have had sex?
15, 19, 21 |
15 - 13%
19 - 72% 21 - 82% |
|
What percentage of people at the following ages still have sex?
57-64, 65-74, 75-85 |
57-64 = 73%
65-74 = 53% 75-85 = 26% |
|
Even if PID is incited by gonorrhea, mixed infections result, and the most common bugs in this mixed infection are:
|
H influenzae and strep pyogenes
|
|
The most severe form of PID is characterized by what?
|
Tubo-Ovarian Abscess (TOA)
|
|
Of all the unintended pregnancies in the US, how many are ended in voluntary abortion?
|
4 in 10
|
|
Of all pregnancies (excluding miscarriages) in the US, how many end in abortion?
|
24%
|
|
Normal semenanalysis values: ejaculate volume
|
greater than 2 mL
|
|
Normal semenanalysis values: sperm concentration
|
greater than 20 million / mL
|
|
Normal semenanalysis values: sperm motility:
|
greater than 50% motile
|
|
Normal semenanalysis values: morphology
|
14% normal
|
|
Normal semenanalysis values: progression
|
greater than 50% normal
|
|
What can capacitated sperm do that un-capacitated sperm can not do?
|
bind to the zona pellucida, increased flagellar beat of the tail, initiate the acrosome reaction
|
|
Which protein within the zona pellucia mediates sperm binding?
|
ZP3
|
|
When the acrosome breaks open, which two enzymes are released?
|
hyaluronidase, acrosin
|
|
What does fertilin do?
|
it is a protein responsible for fusing the membrane of the sperm with the egg
|
|
What is the zona reaction?
|
When the egg releases cortical granules which turn ZP3 into ZP3-F, which prevents additional sperm from fusing into the egg
|
|
What protein holds sperm chromatin in such a condensed form?
|
Protamines, which are specialized histones
|
|
Quick!!! What is the architecture of the sperm's tail?
|
central pair of microtubules, surrounded by 9 pairs of axonemes, surrounded by mitochondria
|
|
What causes the protamines holding the sperm DNA so tightly to relax once the spern enters the egg?
|
oocyte-derived glutathione
|
|
Define "implantation":
|
the attachment of the fertilized egg to the uterine lining, 6-7 days after fertilization
|
|
What part of the conceptus touches the uterine wall first during implantation?
|
the trophectoderm
|
|
How long after ovulation does fertilization occur?
|
12-24 hours
|
|
How long after ovulation does the zygote reach the 2-cell stage?
|
30 hours
|
|
How long after ovulation does the zygote reach the 4-cell stage?
|
40 hours
|
|
How long after ovulation does the zygote reach the early morula stage?
|
80 hours
|
|
How long after ovulation does the zygote reach the advanced morula stage?
|
4 days
|
|
How long after ovulation is the zygote formed into a blastocyst?
|
5 days
|
|
How long after ovulation does the zygote implant into the uterine wall?
|
5-6 days
|
|
When does the blastocyst hatch from the zona pellucida?
|
5 days after ovulation, when the balstocyst reaches the uterus
|
|
What is Decidualization? when does it start?
|
starts in the secretory phase of the menstrual cycle, refers to the endometrial cells becoming round and receptive to the coming zygote
|
|
What are pinopodes? Where are they found?
|
pinopodes are little villi on the endometrial epithelium, that grab the blastocyst and help it implant
|
|
What hormone stimulates formation of pinopodes? What hormone suppresses them?
|
progesterone stimulates pinopodes, estrogen destroys them
|
|
Adhesion of the blastocyst to the endometrial epithelium is mediated by what proteins?
|
integrins, heparin proteoglycans.
|
|
Where is the inner-cell mass in relation to the uterine wall during implantation?
|
The inner-cell mass is on the side of the blastocyst that embeds first
|
|
What happens to the trophectodem cells during the Invasion stage of implantation?
|
They turn into syncytiotrophoblasts and cytotrophoblasts, and extend processes into the endometrium
|
|
Where in the uterus does the zygote usually implant?
|
upper posterior wall
|
|
What is placenta previa?
|
when the zygote implants right close to the cervix
|
|
What is placenta accreta?
|
when the zygote implants over a prior uterine scar
|
|
The most common site of an ectopic pregancy is the......?
|
ampulla of the fallopian tube (80%)
|
|
The second most common site of an ectopic pregnancy is the.......?
|
isthmus of the fallopian tube (12%)
|
|
What are some complications of an ectopic pregnancy?
|
hemorrhage, rupture, maternal death. The fetus is never viable, by the way.
|