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130 Cards in this Set
- Front
- Back
what does the transactivation domain do?
DNA binding? hormone binding? |
transactivation: interacts with RNAP II holoenzyme (TFs, mediators, coactivators, corepressors)
DNA binding: has zinc fingers that bind to HREs (hormone response elements) |
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active Hormone binding domain recruits....
inactive HBD recruits... |
active: HATs
inactive: HDACs |
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where is the glucorticoid receptor located?
where is the estrogen receptor located? thyroid receptor? |
GR: in cytoplasm; when inactive bound to HSP, when active dimerizes and travels to nucleus to bind GRE
ER: in nucleus; ER binding translocates to ERE to recruit HATS and RNAPII TR: already bound to target gene (complexes with HDAC to repress when inactive |
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What is action and purpose of tamoxifen?
ulipristal? |
tamoxifen (selective estrogen receptor modulator SERM): binds the HBD of ER; prevents recruitment of coactivators, thus preventing conformational change of transactivation domain
ulipristal (SPRM): ANTAGONIST; decreases uterine bleeding, fibroid volume (no side effects like with GnRH); can be used for emergency contraception; birth control is also a SPRM antagonist |
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What is action and purpose of flutamide/bicalutamide?
what is a bad thing that can happen if you take this for a while? |
SARM
can be used to treat prostate cancer binds AR, recruits coreppressor protein, shuts down target genes bad: resistance can form resulting in castrin-restistant tumor formation (inactivated androgen receptors mutate and become active again |
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what are the 5 stages of prophase I?
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Leptotene: condensation of replicated chromosomes
Zygotene: synaptonemal complexes Pachytene: completion of synapsis and cross over Diplotene: disappearance of synaptonemal complex (chismata remains) Diakineis: condensation of chroosome for meiosis |
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what is role of Spo II in meiosis?
what bout Rad51/Dmc1? |
holiday model of crossover
SpoII: endonucleus that generates DS breaks Rad51/Dmc1: strand invasion and exchange |
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what is heteroduplex DNA?
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result of Prophase I exchange
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synapsis vs. synaptonemal complex
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synapsis: homologous chromatids pair up during P1 (tetrads)
synaptonemal complex: zipper that tethers homologous chromosomes during P1 |
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chiasmata vs. cohesin?
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chiasmata: homologous chromosomes stuck together
cohesin: holds sister chromatids together |
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primary oocyte arrested in what phase
secondary oocyte |
primary: prophase I; crossing over has occurred but chiasmata still intact (resume at ovulation)
secondary: metaphase II (resume at fertilization) |
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how is metaphase I prevented from happening?
what happens to make the transisition to MI? |
increased cAMP-->PKA--->phosphorylated cdc25 (inactivated) and weel kinase activated (phosphorylates CDK1/cycB-->inactivated)
LH binds receptors on granulosa cells of gaffian follicle results in activation of CDK1/cycB (decreased cAMP levels) |
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why are levels of CDK1/cycb activity decreased after ovulation?
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decreased after M1 so chromosome will remain condensed and nuclear envelope does not form
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how does metaphase II arrest happen?
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Progesterone levels--->Cytostatic factor (CSF) component : MOS blocks APC
MOS uses MAPK pathway resulting in activation of kinase p90rsk--Mad/bub is downstream effector which inhibits APC arrest is due to inability of APC to ubiquinate cyclin B |
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how does anaphase II get initiated?
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sperm binds ovum which causes increase in [Ca]intracellular
APC activated by Ca-dependent phosphorylation APC ubiquinates cyclin B--->degredation-->anaphse II |
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differentiate the two types of spermatagonia A
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stem cells: continuous mitotic dividison
progenitor: divide mitotically several times and remain connected (incomplete cytokenesis) |
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starting with a Type A cell, get to spermatozoa:
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type A stem (mitosis) type A prog (mitosis) type B (one round of mitosis), primary spermatoctye (meiosis I), secondary spermatocyte (meiosis II), spermatid (spermiogenesis), spermatozoa
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what are the gender differences in initiation of meiosis?
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females: entire pop of oogonia initiates meiosis in fetal ovaries; primary oocyte arrested in diplotene stage at P1 prior to birth
male: Type A stem cell pop maintained in testes; @puberty, spermatogonia B initiate meisis continuously |
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gender differences: M1
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female: resume jsut before ovulation; produces 1 haploid secondary oocyte
male: not arrested; produces 2 haploid secondary spermatocyte |
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gender differences M2
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female: coordinated with fertilization; result is 1 haploid ovum
male: MII occurs immeidately after 1st meiotic division; result is 4 haploid spermatid |
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gender differences: recombination frequency
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females 1.7 times more than males
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A 45-year-old woman who is pregnant is concerned that her developing fetus has Trisomy 21 (Down's Syndrome). An amniocentesis is performed and a karyotyping made from the biopsied cells. It is found that the cells show a karyotype consistent with trisomy 21. The time that this chromosomal event probably occurred was during:
A) The fusion of the male and female pronuclei at fertilization B)The first meiotic division of oogenesis C)The second meiotic division of oogenesis D)The first meiotic division of the spermatogenesis E) The second meiotic division of spermatogenesis |
it is most probable that since all of the cells demonstrate trisomy, that the result of this is due to the non-disjunction of chromosome 21 during the first meiotic division of the primary oocyte. While this might also occur during the second meiotic division, it is much more rare. Similarly, it is more atypical that the male gamete undergoes non-disjunction during the meiotic divisions associated with spermatogenesis, or at the time of fertilization.
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The approximate age at which spermatogenesis begins in the life of a male human is
During oogenesis, all of the primary oocytes are formed by what time in the life of the individual? The time at which oogenesis is completed and forms a mature oocyte is |
spermatogenesis: puberty
primary oocyte: birth mature oocyte: fertilization |
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The biopsy of the ovary from an 8-year-old female reveals the appearance of a normal ovary, the cortex of which consisted predominantly of which type of follicle?
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While all of the primary oocytes are present in newborn female infants, these primary oocytes remain as primordial follicles until stimulated by gonadotrophins at the onset of puberty, usually about 11-13 years of age. Therefore, in this example, the biopsy of an ovary from an 8-year-old girl would show a predominance (almost exclusively) of primordial follicles.
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describe the ureter innervation to generate peristalsis?
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PNS (musc) and SNS (alpha)===>GO!
SNS (beta)==>stop! |
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describe the PNS innervation to the bladder?
SNS? somatic? |
PNS (pelvic nerves): motor to detrussor and sensory for distension (both needed to void)
SNS (hypogastric nerves): motor (beta: inhibitatory) to lateral walls of vesical, motor (alpha: excitatory) to internal sphincter at trigone somatic (pudendal nerve): excitatroy input to external sphincter |
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what is the difference between pontine micturition center and cortical control?
what happens when either is hurt? |
pontine: facilitory (destruction: disturbs voiding)
contical center: inhibitatory; voluntary control of restraint (destruction: hyperactive detrussor) |
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how does Benzotropine affect bladder function?
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acetocholinesterase that disrupts the ability of bladder to respond to PNS signals to contract the detrussor
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differentiate the following types of incontinance: stress, urge and bladder
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stress: (women) trauma to sphincters
urge: (prostate) bladder becomes too sensitive (empties too often) blader incontinance: increased bladder volumne overwhelms sphincter |
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contractile dysfunction is (above/below) sacral reflex arc.
noncontracile dysfunction is (above/below) sacral reflex arc. |
contractile: above
noncontractile: below |
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what is the similarity and differences between unhibited bladder and reflex/automatic bladder?
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similarity: contractile dysfunctions
uninhibited: voiding reflex triggered at certain volume; vo(avoid by voiding before magic level) reflex/automatic bladder: no voluntary control, decreased storage capacity; can lead to renal damage |
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describe noncontractile bladder
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paralyzed detrussor, voluntary control lost; pressure overrides sphincter
increased bladder volume |
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Which cells produce a hormone that is responsible for selectively inhibiting FSH secretion?
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granulosa cells produce inhibin
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During sexual intercourse, which gland in the female is responsible for lubricating mucus production?
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The vestibular gland secretes a mucus which provides lubrication for intercourse. The walls of the vagina also become moist as a result of transudation of fluid through the mucous membrane.
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When is genetic sex determined?
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at conception
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what other hormone is required for progesterone to function?
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For progesterone to affect the genital tract, the cells must first have been exposed to estradiol, which induces synthesis of receptors for progesterone.
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how does progesterone affect the uterus?
cervix? when does placenta take over production from CL? |
The structure of human chorionic gonadotropin (HCG) is similar to luteinizing hormone (LH). HCG is responsible for maintaining the CL (corpus luteum) that produces progesterone.
Progesterone relaxes the smooth muscle in the walls of the uterus. This helps prevent premature contractions. Estrogen is thought to prime the uterus for contractions by increasing the number of oxytocin receptors on the muscle. Progesterone keeps the cervix closed. HCG is responsible for maintaining the CL (corpus luteum) that produces progesterone. After ovulation, the follicle fills in with yellowish luteal cells thus forming the corpus luteum. The corpus luteum secretes both estrogen and progesterone to help prepare the uterus for possible implantation. If fertilization does occur, the CL grows and secretes even more progesterone and estrogen to maintain pregnancy. If fertilization does not occur, the CL atrophies leading to loss of hormonal support of the uterus and a new ovarian cycle begins. Placental production of progesterone takes over at week 8 |
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describe how thecal and granulosa cells interact (two cell theory)
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Production of androgens appears to be the main product of the thecal cells. This product, androgen is necessary for the granulosa cells to produce estrogens. The receptors for FSH on granulosa cells interact with FSH to cause an increase in aromatase activity which is necessary to transform androgens to estrogens
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Protection of the oocyte against polyspermy is by a release of factors from the oocyte. Specific granules protect the oocyte from polyspermy. What are those granules called
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Cortical granules extrude their contents into the perivitelline space starting usually at the moment of sperm penetration of the oocyte.
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What is another function of the zona pellucida besides protection of the egg or embryo?
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development of pre-implantation embryo
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What is another name for LHRH (luteinizing releasing hormone)?
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GnRH
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Human chorionic gonadotropin is (hCG) is secreted by what cell type?
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syncytiotrophoblast
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What is the site of rupture of the mature Graafian follicle?
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stigma
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what do the mullerian ducts differentiate into?
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Mullerian ducts in the female differentiate into oviducts and uterine horns. In most mammals, uterus horns remain distinct. In primates and man they fuse to form a simplex type uterus.
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To achieve ovulation, luteinizing hormone must be released in amounts to initiate its effect on the Graafian follicle. What hormone is necessary to initiate the LH surge to initiate ovulation?
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estrogen
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whats in the antrum?
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The antrum is derived as a cavity filled with follicular fluid (liquor folliculi) rich in estrogen. The antrum is formed in the growing follicle and continues to enlarge as it fills with fluid rich in estrogen and the follicle protrudes on the surface as a blister.
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Prolactin causes milk synthesis. Suckling stimulus causes release of prolactin and maintains synthesis and release of prolactin. What parameter does the suckling stimulus inhibit with respect to cyclicity?
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GnRH
thus inhibits LH/FSH |
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how do progestone and estrogen affect breast development differently?
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Progesterone causes growth of lobules and alveoli whereas proliferation of mammary ducts is due to estrogens.
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At the time of ovulation, under estrogen influence, the mucus appears in a pattern when dried. What is the term used for that pattern?
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fern-like
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The first step in synthesis of steroids is derived from the cleavage of cholesterol. What is the enzyme responsible for the cleavage of 20,22-dihydrocholesterol to pregnenolone?
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Delta 5-3 beta-hydroxysteroid dehydrogenase (3 B - HSD)
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Progesterone is converted to 17-alpha hydroxyprogesterone by which enzyme?
androstenedione to testosterone is by which enzyme? |
17 alpha hydroxylase
17 beta hydroxylase |
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Products that help neutralize the acid pH of the vaginal vault are produced by the
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prostate
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In the male, FSH is responsible for stimulating:
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spertatogenesis
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what is the cause of the increase in basal body temp during the luteal phase?
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the increased levels of progesterone raises the set point temperature in the hypothalamus
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ex vivo vs. in vivo vs. in situ
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ex vivo: take cells out, mess with 'em, put em back
in vivo: systemic drug delivery in situ: localized delivery |
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what is the ideal vector as it relates to the following:
reproducibility types of cells it affects site specificity immune response |
easy to reproduce
dividing and non dividing cells sit specific location on host no immune response |
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what are some advantages and disadvantages of adenovirus?
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dsDNA
dividing and non dividing cells disadvantages: nonintegration, transient expression |
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what are some advantages and disadvantages of AAV?
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ssDNA
dividing and non dividing disadvantages: non integration, small capacity transgene expression: potentially long lasting |
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what are some advantages and disadvantages of retro/lentivirus?
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ssRNA, long lasting
disadvantages: cells must be dividing, random integration into genome |
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what are some advantages and disadvantages of herpes virus?
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dsDNA, dividing and non dividing, huge capacity (4X)
disadvantage: no integratio potentially long lasting |
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monosomy
trisomy triploidy tetraploidy mosaism |
monosomy: only one copy of particular chromosome (45)
trisomy: 3 copies (47) triploidy: 69 chromsomes (2 sperm, 1 egg) tetraploidy 92 chromosomes (failure to complete 1st division) mosaism: individual with two cell populations |
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diagnostic screening for trisomy 21
ultrasound bioarkers karyokypes sequencing |
ultrasound: increased fluid
biomarkers: low PAPP-A, high HcG; quad test (alpha-fetoprotein, HCh, estriol, inhibin A) karyotypes: risky b/c may cause miscarriage sequencing: low z score good |
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trisomy 13
18 |
13: patau (47XY, +13)
18: edwards (47XY, +18) |
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Turners
Klinefelters Triple X female XYY |
turners: (45,X)
klinefelters (XXY) triple X and xyy: asymbomatic |
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robertsonian translocation
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fusion of long arms of two acrocentric chromosomes;
short arms are lost (rRNA genes) |
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criduchat
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spontaneous deletion (46,XX, del 5)
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pericentric vs. paracentric inversion
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peri: inversion across centromere
paracentric: inversion w/in one area of chromsome |
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At which stage in the menstrual cycle are the endometrial glandular cells maximally developed and stimulated?
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late secretory
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trisomy 21:
what is the result when nondisjunction occurs in M1? M2? |
M1: 2 trisomy gametes, 2 monosomy
M2: 2 normal gametes, 1 trisomy, 1 monosomy |
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where are leydig cells found?
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in the intertubular cpace of the seminferous tubules
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what is the difference between type A and type B spermatagonia?
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type a: oval euchromatic nucleus/nucleolus attached to nuclear envelope
type b: round nucleus, masses of heterochromatin and central nucleolus (dark in middle and not so dark patches on the outside) |
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how long does spermatogenesis last:
what are the three parts of sperm development |
64 days
1. spermatogenesis: spermatozoa to spermatocyte 2. meiosis: spermatocyte to spermatid 3. spermiogensis: spermatid to spermatozoa |
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what happens in the following spermiogenesis phases:
golgi phase cap phase acrosomal phase maturation phase |
golgi: polarize (acrosomal vesicle on side and centrioles on the other)
cap: acrosomal sac flattens and descends around nucles; centriolar pair forms axoneme; SPERMATID ROTATES 180 degrees (tail out!) acrosomal stage: mancheete develops and moves caudally; mito align along axoneme maturation: manchete does its thing and disappears, residuals bodes eaten by sertoli cells; CHROMATIN CONDENSES |
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how does prolactin affect leydig cells?
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induces expression of LH receptor
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what cells population marks the transition from seminferous epithelium to tubulus rectus?
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columnar sertoli cells
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describe the rete testis epithelium? what about the interluminal androgen concentrations?
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simple cuboidal epithelium
lots of androgens (good b/c ABP released by sertolis) |
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describe the efferent ductule epithlium?
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scalloped outline
priniciplel cells with microfilli and ciliated cells (to propel sperm) |
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describe the epididymis epithelium.
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principal cells with sterocilia and basal cells
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how can you distinguish the vas deferens?
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lots of smooth muscle
narrow lumen pseudostratified columnar with sterocilia |
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how can you distinguish the seminal vesicles?
what is their purpose? |
lots of vacuoles; lots of fructose, proteins and prostiglandins
capacitates sperm |
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what is BPH?
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noncancerous enlargement of prostate gland that can restrict flow of urine through prostatic urethra
nodules in mucosal glands |
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what reaction does 17-HSD catalyze?
desmolase Star which is RL enzyme? |
17-HSD: Androstenendione to Testosterone
Desmolase: cholesterol to pregnenolone staR: cholesterol esters to Desmolase/SCC (RLS) |
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what happens to testicles and sperm production if FSH is reduced?
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decreased ball size and decreasesd sperm production
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descibe the fetal and pubertal targets of T
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fetal: TUBING; epididymis, vas deferens, seminal vesicle
puberty: YOUNG MAN; penis, seminal glands, musculature, skeleton, larynx SPERMATOGENESIS |
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describe the fetal and pubertal targets of DHT?
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fetal: EXTERNAL; penis, penile urethra, scotum, prostate
puberty: OLD MAN; scrotum, prostate, sex hair, sebaceous glands, prostatic secretions |
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what is an inhibitor of 5 alpha reductase? what is it used for?
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finasteride
prostatic hyperplasia, hirsutism, and acne |
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what 3 hormones are necessary for normal spermatogenesis?
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FSH, LH, T
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how do sertoli cells produce estrogens?
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they lack desmolase
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what hormone is affected when Sertoli cells secrete inihibins/activins?
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FSH secretion from pituitary
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what cells produce androgen binding proteins?
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sertoli cells
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what cells express MIS (embryo)?
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antimullerian hormone
sertoli cells |
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what is the preferred energy source for sperm development? where is it produced?
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lactate from sertoli cells
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how are leydig cells stimulated before they develop pituitary glands?
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placental hCG stimulates them then pituitary LH
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how do bones use estrogen for growth?
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bones have aromatase, specifically at the epiphyseal plate
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What binds Androgen Receptor (AR) on target tissues? what binds with highest affinity?
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T and DHT
DHT with higher affinity |
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cavernosal nerve is what category of neuron?
what is its job? |
carernosal nerve: NANC (not adregenic, not cholinergic)
increases NO---->activates GC--->cGMP--->lowers intracellular calcium--->vasodilation phosphodiesterase breaks down cGMP |
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differentiate Precocious Puberty and Pseudopuberty
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prococious: hypersecretion of T, premature development (INCREASED REPRODUCTIVE CAPABILITY)
pseudo: increased T via adrenal cortex (NO REPRODUCTIVE CAPABILITY) |
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DESCRIBE THE sperm of someone taking a T Rx?
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decreased sprerm density
increased T will descreases LH and FSH |
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differentiate 5 alpha reductase deficiency and androgen receptor defect.
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5ar: decreased DHT, female phenotype at birth and virilization at puberty (increased facial hair, masculinity)
AR defects: decreased androgenization despite normal DHT |
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Complete Androgen resistance
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46XY, female phenotype, blind ending vaginal pouch
at puberty: female secondary sex characteristics, boobs, no period, no pubic/axillary hair! Testes in intrabdominal cavity or labial folds |
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what hormones regulates steroid synthesis in the ovary?
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LH
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CYP11A1 aka
17 Beta HSD aka |
desmolase
aromatase |
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what enzyme is needed to make progesterone from pregnenolone
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3 beta HSD
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how do granulosa cells produce estrogen?
how are LH and FSH needed? |
androgens made from thecal cells diffuse into granulosa cells.
aromatase converts androstendione to estrone and 17BHSD1 converts estrone into estradiol-17beta |
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besides upregulate progesterone and estrogen for cholesterol uptake, how does LH help maintain corpus luteum
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increases cholesterol uptake for steroid synthesis
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how are estrogens and progesterone transported in blood?
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estradiol/estrone: SSBG
progesterone: Corticosteroid binding protein |
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what are responsible for sex hair and sebaceous gland development?
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ovarian androgens
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what is thought to be upregulated at puberty, stimultaing GnRH secretion?
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kisspeptin
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how do you treat a girl with precocious puberty
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progestational agents
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how does contraception and menopause differ in relation to FSH/LH levels
why do old ladies start looking like dudes later on in life? |
contraception: low FSH/LH (via negative feedback from estrogen and progestin)
Menopause: high FSH/LH (from low estrogen and low inhibin) ovaries still secrete androgens |
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hCG, in both males and females, acts like.....
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LH
maintains corpus luteum in girls stimulates T synth in bros |
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what is the purpose of hCS/hPL?
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levels increase as placental mass increase
increase supply of glucose, FFA and ketones to fetus can result in gestational dibatetes |
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what is source of progestrone in women during pregnancy?
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C until week 6-8: CL
after week 8: placent is main source |
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how does placenta make estrogen?
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placenta lacks CYP17 (can't make DHEA from progesterone)
relies on androgens from fetus/mom DHEA-S |
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what hormones help out during parturition
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PCRH increased, prostiglandins increased, oxytocin increased
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where are oxytocin and prolactin made and released?
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oxytocin: made in the hypothalamus, released in posterior pituitary
prolactin: made anterior pituitary from GnRH stimulation |
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describe how prolactin is normally regulated and how it gets released
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normally under tonic inhibition from dopamine
pregnancy: estrogen increases PRL secretion and decreases dopamine response VIP and thyrotopin releasing factor (TRH) also are positive lactotrophs |
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how does prolactin affect breasts?
why doesn't lactation begin until after parturition? |
increases breast development
progesteron and estradiol fall at partiution, which removes disinhibition of lactalbumin and casein synthesis |
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what is lactational amenorrhe?
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lactation increases which results in a decrease in GnRH pulses
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how do you treat prolactinomas?
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dopamine agonists
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where does oxytocin synthesis occur? what is included in the prohormone?
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PVN
neurophysin I |
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what triggers oxytocin release? how does oxytocin help with contractions?
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released from cervical stretching; lowers theshold for depolarization in uterine muscle.
increase in intracellular calcium, MLCK increases in Force and number of uterine contrations |
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how is oxytocin related to myoepithelial cells in breasts?
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oxytocin: ejection
prolactin: secretion |
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Fragile X syndrome affects the ability of ______ gene to code for _____
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FMR1 to code for FMRP
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differentiate premuation and full mutation of fragile X
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premutation: 55-200 repeats, (POI, FXTAS), high transcription, low translation (hairpin)
full mutation: >200 repeats, hypermethylation, condensation, transcriptional silencing, |
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what is the expressive difference between female carriers of fragile x and male carriers?
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males got it bad
|
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what does the FMRP do?
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RNA binding protein
binds specific mRNA's for axon function and mGluR |
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differentiate normal, intermediate, premutation and full mutation for fragile X syndrome
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CGG repeats
normal <45 int: 45-54 pre: 55-200 full: >200 |
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2 possible causes for fragile x
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1. Meiosis
unequal crossing over in P1 of meiosis (2 screwed up) P2: 1 screwed up 2. misparing during DNA replication, bypasses DNA repair mechanism and gets expanded during next roudn |
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how do norepi, kisspeptin and dopamine affect GnRH release from the median eminance?
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norepi and kisspeptin increase
dopamine inhibit |