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PHSI 208 > repro > Flashcards

repro Flashcards

1
Q

what is nondisjunction?

A

when chromos do not separate properly after division

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2
Q

what are the various types of abnormal sex distribution syndromes?

A 
Klinefelters, XXY; 
Turner's syndrome, X
Y is non viable
XYY...
XXX-->no distinct phenotypes
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3
Q

when do repro structures differentiate?

A

seventh week of development –prior to this time they are considered bipotential

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4
Q

Male or female development depends on the presence or absence of sex determining region of the Y chromosome (SRY gene)

A

ya

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5
Q

how to the bipotential gonads form female gonads?

A

gonadal cortex forms ovary while the medulla regresses; wollfian duct also regress because of lack of testosterone; mullerian duct becomes fall tube, uterus, cervix, and upper half of vag

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6
Q

how to the bipotential gonads form male gonads?

A

gonadal cortex regresses; medulla forms testis; wolffian duct forms epididymis, vas def, and seminal vesicles (presence of testosterone); mullerian duct regresses due to AMH

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7
Q

how does the SRY gene dictate sex?

A

SRY gene produces TDF (testis determining factor)–>creates SOX9, WT1, SF1–.guides development of gonadal medulla into a testis; testes then produce:

  • Anti-Mullerian hormone (sertoli cells): causes mullerian ducts to regress
  • Testosterone (leydig cells): converts Wolffian ducts into male accessory structures (epididymis, vas deferens, and seminal vesicles)
  • Dihydrotestosterone (leydig cells): differentiation of external genitalia–development of prostate
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8
Q

what causes formation of external genetalia?

A

External genitalia development driven by presence or absence of androgens (DHT)

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9
Q

describe female gametogenesis

A

during embryogenesis, oogonium undergo mitosis then meosis I–generate primary oocytes; at puberty, primary oocyte splits into secondary oocyte and polar body; secondary oocyte released as egg during ovulation, then will complete meiosis II when fertilized

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10
Q

describe GnRH release

A
  • Released from hypothalamus in pulsa)le fashion every 1-3 hours in both sexes
  • -females also have a surge corresponding with ovula)on
  • children with a GnRH deficiency will not mature sexually without gonadtrophin s)mula)on of the gonads
  • synthe)c GnRH must be delivered in a pulsa)le manner
  • constant delivery of GnRH leads to down regula)on of receptors in the pituitary gonadotropes
  • high GnRH treatment for certain breast or prostate cancer
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11
Q

what is the erectile tissue of the penis?

A
  • Corpus spongiosum

- Corpora cavernosa

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12
Q

what is involved in prostate development?

A

DHT

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13
Q

how can prostate cancer be treated?

A

-administra)on of 5a-reductase inhibitor (finasteride) blocks DHT production, shrinks hypertrophied prostate

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14
Q

describe the seminif tub

A
  • -site of sperm production
  • -Developing spermatocytes stack in columns from outer edge to lumen with sertoli cells between each column
  • –found in inters))al )ssue produce testosterone during development then again ader puberty
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15
Q

Basal lamina of seminif tubule keep out large par)cles but allows testosterone to enter

A

improtant for developing sperm

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16
Q

describe sertoli cells

A
  • cntain tight junction with adjacent sertoli cells forming a blood- tes)s barrier between tubule lumen and inters))al space
  • regulate sperm development -“sustentacular cells” provide sustenance or nourishment
  • Produce a variety of substances: hormones (ac)vin & inhibin); growth factors; enzymes; and androgen binding protein (ABP) which binds to testosterone to keep it in the tubule lumen
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17
Q

describe how GnRH neurons activate to release hormones

A

GnRH-containing neurons are cyclically activated to fire APs–>release trophic hormones (GnRH) which are released into the first capillary bed; they are then carried to endocrine cells with GnRH receptors in anterior pit gland where a second cap bed lies; they acts on endocrine cells to release their peptide hormones–>LH and FSH–>enters blood stream and goes to gonads

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18
Q

what is the blood testes barrier

A

a lining of sertoli cells which provide a barrier between the blood and seminif tubs; improtant, because gametogenesis is very sensitive–xenos in blood could destroy developing sperm

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19
Q

where do spermatids compete transformation, and what occurs?

A

–remain embedded in apical membrane of sertoli cells–>lose most cytoplasm, form a flagellum; chromatin condenses, acrosome forms and caps the nucleus; a mid piece forms which is needed for energy (contains mito);

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20
Q

how long does it take to go from spermatogonium to free sperm?

A

64 days, with 200 million produced

21
Q

where do sperm mature?

A

-mature in the epididymis (epididymal cells secrete proteins) during 12 or so days of transit time

22
Q

what hormones does spermatogenesis require?

A
  • FSH binds to receptors on sertoli cells causing them to generate paracrine molecules needed for spermatogonia mitosis and spermatogenesis
  • also produce ABP and inhibin
  • LH targets the inters//al leydig cells resul)ng in produc)on of testosterone -essen)al for spermatogenesis and ac)ons appear to be through sertoli cells but exact mechanism not completely understood -spermatocytes do not have receptors for FSH, LH or androgens
23
Q

what do the accessory glands excrete which contribute to the composition of semen?

A
  1. Nutrients
  2. Buffers for protec)on against acidic vaginal
    environment and residual acidic urine in urethra
  3. Chemicals to increase sperm mo)lity
  4. Prostaglandins (mo)lity and contrac)on of male and female reproduc)ve tracts)
  5. Immunoglobulin’s, lysozyme and other an)bacterial compounds
24
Q

what are the primary sex characteristics (men)?

A

Primary sex characteris/cs: internal sexual organs and external genitalia, which we learned are differen)ated to male during embryonic development by androgens and their growth afer puberty is also due to androgens.

25
Q

what are the secondary sex characteristics?

A

Secondary sex characteris/cs: facial and body hair growth, muscular development, thickening of vocal chords (lowering of voice) and behavioral effects i.e. sex drive (libido)

26
Q

Androgens are anabolic hormones and promote protein synthesis
-brain -kidneys -heart -skin -liver

A

ya

27
Q

vulva/pudendum–external female genetalia

A

ya

28
Q

what are the layers of the uterus?

A

perimetrium–thin outer connective tissue
myometrium– thick layer of smooth muscle
endometrium–inner layer

29
Q

how do the fall tubes move eggs down to the uterus?

A

through 2 layers of sm muscle and cilia

30
Q

what are th phases for ovarian cycle?

A 
Follicular phase: marked by follicular growth, variable 10 days to 3 weeks
Ovula/on: once one or more follicles have ripened, the ovary releases oocyte(s) during ovula)on
Luteal phase (post ovulatory phase): ruptured follicle transforms to corpus luteum (yellow), named for yellow pigment and lipid deposits. -secretes hormones, ceases to func)on afer two weeks if no implantation
31
Q

what is the antrum?

A

a liquid component of the tertiary follicle whcih contains enzymes

32
Q

describe the phases of the uterine cycle

A

menses–0-7
proliferation-7-14 (latter part of the follicular phase, the uterus adds new cells to the endometrium layer in an)cipa)on of pregnancy)
secretory phase–14-28– (after ovulation hormones from corpus luteum covert thickened endometrium into a secretory structure
-if pregnancy does not occur the superficial endometrium layers are lost during menstruation and the cycle begins again)

33
Q

Hormonal control of the menstrual cycle is complex

  • GnRH from hypothalamus
  • FSH and LH from the anterior pituitary -Estrogen, progesterone, inhibin and AMH from the ovary
  • During the follicular phase estrogen is dominant
  • ovula)on is triggered by surges in LH and FSH -during luteal phase progesterone dominant
A

ya

34
Q

vasectomy cauterizes/ties and cuts the vas deferens

A

VASectomy

35
Q

how do hormonal contraceptives work for women?

A

Various combina)ons of estrogen and progesterone inhibit gonadotropin secre)on (LH and FSH) from the anterior pituitary necessary for ovula)on. Progesterone also thickens cervical mucus

36
Q

what is RISUG/VasalGel?

A
  • reversible inhibi)on of sperm under guidance
  • injec)on of polymer gel into vas deferens
  • -gel may create acidic enviro toxic to sperm;
37
Q

what can infertility arise from in men?

A

abnormal sperm motility, abnormal sperm in general, low sperm count, infections/scar tissue, retrograde ejac, sperm antibodies

38
Q

what can infertility arise from in women?

A

damages fall tubes, (scar tissue);
ovulation disorders–hypothalamic dysfunctions; premature menopause, PCOS
endometriosis–scar tissues
cervical stenosis–polyps or fibroids grow on uterus or endometrium and prevent implantation

39
Q

what controls sperm to capacitate?

A

substances in uterus–albumin, lipoproteins, proteolytic enzymes

40
Q

when can an egg be fertilized after ovulation?

A

An egg is viable to be fer)lized for 12-24 hours post ovula)on

41
Q

where does fert occur?

A

in distal portion of fall tub

42
Q

developing follicle releases estrogen–contributes to proliferation of endometrium; when the ovum is released from the follice, endometrial thickness stagnates; the corpus luteum forms and gives of progesterone (and estrogen) which maintains endometrial thickness; when there is no implantation, corpus luteum disintegrates and endometrium can no longer be maintained without progesterone–sheds

A

ya

43
Q

which cells in the follice contain LH and FSH receptors?

A

theca cells contain LH receptors, granulosa cells contain FSH receptors

44
Q

describe the early to mid follicular phase

A

First day of menstrua)on is day 1

  • FSH and LH released, several ter)ary follicles mature
  • Granulosa (FSH) and thecal (LH) cells begin to produce hormones
  • Androgens (androstenedione) converted to estrogens (aromatase) in granulosa cells -AMH prevents addi)onal follicle recruitment -estrogen nega)ve feedback anterior pituitary, posi)ve on granulosa cells -estrogen causes endometrium prolifera)on
45
Q

describe the late follicular phase

A
  • estrogen release peaks from follicles -some follicles undergo atresia, dominant follicle persists and granulosa cells now begin to also release progesterone and inhibin
  • persistently high estrogen flips to posi)ve feedback on hypothalamus
  • LH surges to greater degree than FSH (inhibin)
  • high estrogen readies endometrium of uterus for implanta)on
46
Q

describe ovulation

A

occurs 16-24h after LH spike
–LH needed for final steps of oocyte maturation
meosis resumes
Mature follicle secretes prostaglandins and proteoly)c enzymes -proteoly)c enzymes breakdown collagen and connec)ve )ssue holding follicle together–break out of ovary as well
-prostaglandins may contribute to rupture of follicle and/or ovary wall
-secondary oocyte is swept into fallopian tube by fimbriae

47
Q

describe early-to mid luteal phase

A

Both thecal and granular cells transform into luteal cells

  • lipid droplets and glycogen granules accumulate in cytoplasm and it begins to secrete progesterone -estrogen and progesterone levels steadily rise and provide nega)ve feedback to hypothalamus and anterior pituitary
  • progesterone (dominant during luteal) con)nues to influence endometrium (secretory) in prepara)on for pregnancy
  • cervical plug preven)ng bacteria and sperm
48
Q

describe the late follicular phase

A

Corpus luteum has life span of ~12 days
-if pregnancy does not occur, spontaneous apoptosis, to become corpus albicans -progesterone and estrogen fall, FSH and LH increases
-maintenance of endometrium depends on progesterone, when it decreases, vessels in surface contract causing surface cells to die -about 14 days aRer ovula)on, 2 days aRer corpus luteum ceases func)on menstrua)on begins -40ml blood, 35 ml of serous fluid and cell debris
surge in LH causes thinning of mucus—more water—sperm can pass through and fertilize the egg

PHSI 208 (32 decks)

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