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Physio Exam 3 - Endocrine > 22 | Reproduction > Flashcards

22 | Reproduction Flashcards

1
Q

genetic sex

A

defined by karyotype

  • 44 somatic chromosomes
  • XX (female)
  • XY (male)
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2
Q

gonadal sex

A

defined by internal genitalia, due to genetics

  • SRY (sex determining region) induces testis development
  • both Xs required for ovarian development
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3
Q

turner syndrome (XO)

A 
XO (also ovarian agenesis)
-underdev. gonad
-amenorrhea (no menstrual) 
-short stature, webbed neck 
-lack secondary sex characteristics 
(YO lethal)
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4
Q

jacobs (XYY)

A

XYY (super male syndrome)

  • seemingly normal male
  • excess acne, taller, more aggressive
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5
Q

kleinfelter’s syndrome (XXY)

A 
XXY (seminiferous tubule dysgenesis) 
-male genitalia
-inc FSH, LH, E2 
-dec T 
-sterility, feminization, retardation 
"hypergonadotropic hypogonadism"
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6
Q

triple X syndrome

A

XXX

-no unusual abnormalities, only one X chromosome remains active

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7
Q

phenotypic sex

A

defined by genital ducts + external genitalia + secondary sex characteristics
-fetal steroidogenesis supported by hCG in both sexes

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8
Q

male phenotypic sex

A
  • sertoli cells produce Mullerian Inhibiting Hormone (growth factor)
  • MIH causes regression of Mullerian ducts
  • Leydig cells produce testosterone
  • T supports differentiation of Wolffian ducts (precursor of epididymis, vas deferens, seminal vesicle, ejaculatory duct)
  • conversion to DHT, induces prostate, urethra, penis, scrotum
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9
Q

female phenotypic sex

A
  • lack MIH + testosterone
  • Mullerian ducts develop, Wolffian ducts regress
  • develop oviduct, uterus, vagina
  • female external genitalia appear by labial growth
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10
Q

male sexual development

fetus, post natal, adolescent, adult

A
  • T synth at adult levels by end of first trimester (leads to differentiation of internal and external genitalia) + again at 2 mo
  • low levels until puberty, hypothalamus active again, less sensitive to T inh (reset gonadostat) leading to inc T
  • growth of penis, sebaceous glands, axillary + pubic hair
  • T levels max in 20s, gradually fall after
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11
Q

female sexual development

fetus, post natal, adolescent, adult

A
  • estrogen synthesis during gonadal dev. at end of first trimester
  • FSH, LH high 2-3 mo
  • rise again at puberty
  • breast dev. (therlarche)
  • axiallary + pubic hair (pubarche)
  • menarche
  • E levels peak monthly after menarche
  • periods irregular (climacteric)
  • cease in 50s (menopause
  • post-menopausal LH + FSH high b/c of low E and lack of inhibin
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12
Q

sex steroids + growth (both sexes)

A
  • long bone growth augmented (E or T–> E)
  • high levels near end of puberty close epiphyseal plate
  • 8 to 10 years, adrenals inc androgen secretion (adrenarche) w/out sig changes in cortisol or ACTHlevels
  • androgens (from androstendione) role in early growth spurt, pubic + axillary hair growth, ind of gonadal puberty
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13
Q

androgen insensitivity syndrome

A

(testicular feminization)

  • XY genotype, female external genitalia
  • due to no functional androgen rec.
  • Mullerian ducts regress w/ MIH, but Wolffian ducts also regress b/c can’t respond to T
  • Leydig cells produce T, but Sertoli cells can’t function so no spermatogenesis
  • later w/out neg feedback from T, inc in GnRH to LH to A to T to E (peripheral aromatization)
  • breast development, female phenotype even though T>E
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14
Q

5a-reductase-2 deficiency syndrome

A

(penis at twelve)

  • XY genotype, begins life w/ female phenotype, later reverts to male phenotype
  • 5a-reductase-2 gene is non-functional
  • Y chromosome leads to testes and internal male ducts b/c T is present, but no prostate, penis or scrotum form since DHT is required
  • at puberty inc T may bind enough to receptor to induce development of external male genitalia, and/or 5a-reductase-1 present in prostate and external genital tissues may be enough w/ very high T
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15
Q

congenital adrenal hyperplasia (CAH)

M+F

A
  • females: masculinization (enlargement of clitoris, fusion of labia before birth, inc mucular dev., facial hair (hirsuitism), irregular menses post-puberty)
  • males: precocious puberty or supermasculinization
  • due to hypersecretion of adrenal androgens w/ defect in steroid biosynthesis
  • 21- or 11B-hydroxylase deficiency reduces formation of aldosterone and cortisol, leads to build up of androgen precursors
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16
Q

cells of the testis (3)

A
  1. spermatogonia (germ cells): sperm prod. stem cell line
  2. leydig cells (interstitial): stimulated by LH, synthesize + secrete T
  3. sertoli cells (follicular): stimulated by FSH (+T to prod ABP). surround and nurse dev. sperm
    - interconnected laterally by tight junctions, form “blood testis barrier”
    - lots of aromatase and can convert T to E2
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17
Q

testosterone effects (3)

A
  1. fetal: induce Wolffian duct system directly. induce prostate and urethra/penis/scrotum via DHT (through 5a-reductase-2)
  2. puberty: induce facial, pubic + axillary hair; sebaceous glands (mainly via DHT); sperm prod; larynx dev; fat + muscle distribution; bone growth during puberty but ends bone growth by inc T post-puberty (T acts indirectly by aromatase-med conversion to E)
  3. adult: sex drive; muscle growth + maintenance (T is anabolic steroid); inc erythropoiesis (inc male hematocrit); inc male baldness (via DHT); inc cholesterol with neg CVS consequences
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18
Q

oligospermia

A
  • less than 20mil sperm/mL (1/5)

- due to dec GnRH (anabolic steroid abuse; stress), poor nutrition, enviro factors

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19
Q

defective sperm

A

even with sufficient number, may be physically defective, not motile or later capacitation, hyperactivation, or acrosome reaction
->50% defective is problematic

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20
Q

male contraception?

A

difficulties: 2 mo for sperm production, sheer number
- possibility of GnRH or gonadotropin antagonists; T analog; progesterone; inh of sperm motility or function; blockage or sperm-egg reaction

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21
Q

impotence

A

erectile dysfunction

  • anti-ACh drugs, nerve damage, aging cant inh arteriolar dilation via NO path
  • drugs selective inh of phosphodiesterase-5, hydrolase which hydrolyzes signaling molec for cGMP in Ca2+ channel closure. inc cGMP, dec IC Ca2+, smooth muscle relaxation, erection
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22
Q

benign prostatic hyperplasia (BPH) + male pattern baldness

A
  • since T must be converted to DHT for prostate growth + maintenance, specific inh of 5a-reductase-2 with finasteride (T analogue) used to treat BHP
  • reversal of scalp hair loss
  • higher dose for prostatic hyperplasia and lower for MPB
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23
Q

cells of the ovary (3)

A
  1. oogonia (germ cells): exist only during fetal life, generating fixed number of primary oocytes by birth.
  2. theca cells (interstitial): stimulated by LH to produce androstenedione. theca cells are low in aromatase, can’t effectively convert androgens to estrogens.
  3. granulosa cells (follicular): surround and nurse developing oocytes. stimulated by FSH to produce abundant aromatase, can convert theca cell androstenedione to estrogen.
24
Q
  1. early follicular phase

hormones - menstrual cycle

A

(were strongly inh by P, E + inhibin A)

  • LH + FSH rise as P, E + inhibin A dec
  • uterine lining degenerates, no longer supported by P, menstruation
  • stim by FSH, no follicles begin to dev. proliferating granulosa cells sec inhibin B
25
Q
  1. mid follicular phase

hormones - menstrual cycle

A
  • increasing inhibin B begins to suppress FSH release
  • as FSH dec, one follicle dominates, other atresia
  • E levels inc b/c of LH stim theca cell prod of androgens, then granulosa cell conversion of androgens to E w/ FSH-induced aromatase
  • E stim more growth of granulosa and theca cells (autocrine + paracrine)
26
Q
  1. late follicular phase

hormones - menstrual cycle

A
  • E ind growth of follicle, rapidly inc E levels, stim more follicular growth
  • inc E makes anterior pituitary inc more sensitive to GnRH by inducing more GnRH receptors on gonadotrophs, “positive feedback”
  • LH release inc quickly (GnRH maybe too)
  • E (+FSH) ind LH rec on granuosa cells that surround oocyte
27
Q
  1. ovulation

hormones - menstrual cycle

A
  • rapid inc in LH triggers ovulation through action on now-LH-sensitive granulosa cells
  • granulosa cells release lytic enzymes and PGs to expel oocyte
  • passive release (co-sec) of FSH and then inhibin B response
  • LH surge also induces completion of oocytes first meiotic division, prep for fertilization
28
Q
  1. early luteal

hormones - menstrual cycle

A
  • LH surge and loss of oocyte signaling to follicle cause metabolic shift
  • after “luteal” cells produce less E and inhibin B, but inc amount of P and inhinbin A
29
Q
  1. mid luteal

hormones - menstrual cycle

A
  • as corpus luteum grows under LH stim - P, E, inhibin A rise max
  • but resulting inc of P with E inhibits GnRH and LH release, while inhibin A inh FSH
30
Q
  1. late luteal

hormones - menstrual cycle

A

(if implantation occurs, trophoblasts of embryo produce hCG (~LH), which maintains corpus luteum for first 2 months of pregnancy, if not..)

  • corpus luteum lack LH - (lutenizing hormone) degenerates
  • P, E and inhibit A levels dec quickly
  • release hypothalamus and anterior pituitary from inhibition
31
Q

8 –> 1. end cycle/recycle

hormones - menstrual cycle

A

-lacking inh FSH an LH begin to rise, stim new cohort of follicles

32
Q
  1. menstrual phase

uterine events - menstrual cycle

A

(days 1-5)

  • from initiation to completion of bleeding
  • epithelial lining of uterus (endometrium) degenerates and sloughs off
  • results in menstrual flow (menses)
33
Q
  1. proliferative phase

uterine events - menstrual cycle

A

(days 5-14)

  • under influence of inc E, endometrium regenerates, thickens, forms glandular structures
  • induced by inc E, progesterone receptors appear on endometrial cells
  • underlying myometrium (smooth muscle) thickens and also gains P receptors
34
Q
  1. secretory phase

uterine events - menstrual cycle

A

(days 14-28)

  • under influence of inc P: mucus + fluid secretion, glycogen synthesis + vascularization increases
  • while P inhibits myometrial contraction in prep for implantation
35
Q

mid-cycle

cervical mucus

A
  • under influence of E, cervical mucus initially thin, allowing sperm movement
  • but under influence of inc P, cervical mucus thickens + becomes acidic, preventing sperm movement + bacterial invasion
36
Q

end-cycle

endometrium

A
  • fall in E and P deprive endometrium of support, cause constriction of uterine blood vessels, reduced blood flow, PG secretion and eventual death of the tissue
  • w/out inh by P, myometrium rhythmically contracts, + endometrial blood vessels dilate
  • hemorrhage through weakened capillary walls
37
Q

effects of estrogen (females)

stim - 7, inh 3

A 
[stimulate]
-growth + maintenance of reproductive tract + female body 
-bone growth + maintenance, epiphyseal plate closure 
-pubic hair pattern
-cervical mucus sec
-breast dev + function 
-prolactin sec 
-myometrial contractions
[inhibit]
-GnRH release (moderate E in early to mid, follicular; E+P in luteal) 
-milk producing effects of prolactin 
-atherosclerosis (dec cholesterol?)
38
Q

effects of progesterone (females)

stim - 4, inh 3

A 
[stimulates]
-breast glandular growth
-uterine secretion
-cervical mucus thickening 
-increase in body temp 
[inhibits]
-GnRH release
-myometrial contractions 
-milk-producing effects of prolactin
39
Q

why do estrogens have dif effects, at dif times, on dif tissues?

A
  • two estrogen receptor genes, ERa + ERb
  • expressed differentially + can associate with different co-activators or co-repressors
  • these can trigger different signaling pathways with different outcomes
40
Q

issues with hormone replacement therapy in females

A
  • E supplements can be given to alleviate menopausal symptoms and preserve bone mass
  • but long term HRT can inc risk of certain breast and endometrial cancers, have adverse CVS consequences (stroke, MI, pulmonary emboli, DVT)
  • breast cancer in hysterectomized women ins’t sig inc by estrogen supplements
  • E+P req to minimize uterine cancer risk in normal women but at and inc risk of breast cancer
41
Q

predicting ovulation (4)

A
  1. observe menstrual cycle
    - egg is viable for ~1 day, sperm for 2-4 days. narrow window to result in conception.
  2. influenced by circadian + external factors. avg inc of 0..5 degrees C in body temp after ovulation, through luteal phase. thermogenic effect of P.
  3. before ovulation vaginal mucus is thin but string. vaginal smear dries with branching salt crystals. after ovulations is highly viscous, no crystals.
  4. track and record daily estradiol and progesterone metabolites in urine average over several menstrual cycles.
42
Q

promoting ovulation/fertilization (2)

A
  1. ovulation induction
    - E2 agonist -> inc GnRH -> GSH
    - hMG (human menopausal gonadotropin) = FSH+LH) or FSH stimulation
    - phased protocols, administration of FSH while blocking normal cycle with GnRH antagonist + terminating with pulse of hCG to trigger (multiple) ovulation
  2. assisted reproductive technologies (ART): IVF and ICSI (intracytoplasmic sperm injection) use multiple oocytes obtained by induction protocols, fertilized by capacitated or injected sperm, respectively.
43
Q

hormonal birth control: progestin only

A

-daily oral dosage
-DMPA, depomedroxyprogesterone acetate injection 4x/year
-levonorgesterel implant, lasts 5 years
[dec LH, FSH + E2 to early/mid follicular phase range, suppressing ovulation and producing thick cervical mucus and thin, atrophic endometrium. can allow irregular bleeding]

44
Q

hormonal birth control: combination estrogen + progestin

A

-oral daily (21 days on/7 off or placebo)
-monophase: constant E/P ratio
-biphasic: two dif E/P ratios
-triphasic: 3 dif E/P ratios
[phased dosages produce more normal uterine phases, but still suppress ovulation, sperm entry + fertilization]
-E+P can also be given monthly by injection or weekly by transdermal paths
-extended cycle oral protocol gives 4 periods/year

45
Q

hormonal birth control: morning after

A
  • 2 doses of progestin, 12 hours apart within 12 hours of intercourse
  • function is same way as progestin-only contraceptive, depending on when its take in menstrual cycle
46
Q

sperm development (3)

A

after ejaculation, sperm undergo changes in female reproductive tract to function

  1. capacitation: epididymis-derived proteins stripped off; transmembrane proteins rearranged; metabolism + motility also inc (req for IVF)
  2. hyperactivation: receptor-mediated Ca influx converts slow, wave-like beating to rapid, whip-like beating, triggered by proximity to egg - paracrine signal
  3. acrosome reaction: sperm head binding to zona pellucida, triggers exocytosis or trypsin-like proteolytic enzyme (acrosin) from acrosome, clears path for sperm head to fuse w/ egg plasma membrane
47
Q 
chorionic gonadotropin (CG or hCG) 
[placental hormone]
A
  • produced by trophoblasts almost immediately after their invasion into endometrium
  • signal from embryo that implantation has occurred
  • structurally and functionally similar to LH, CG maintains corpus luteum for up to 2 months, strongly stim P + E production, preventing further ovulation
  • CG peaks after !3 months, then declines to near-constant level until delivery
  • detection in urine used for home pregnancy tests
48
Q

progesterone (P)

[placental hormone]

A
  • made at first by corpus luteum, later by placena
  • critical for maintain uterus in receptive condition for implantation, breast development, and inhibiting uterine contraction during pregnancy
  • after corpus luteum degeneration, level increases, but efficacy of inhibition decreases and parturition approaches

RU486: competitive inhibitor of P, causes endometrial degradation and myometrial contraction. if administered wit a prostaglandin, results in expulsion of fetus.

49
Q

estradiol/estriol (E2/E3)

[placental hormone]

A

-cooperative products of fetal adrenal synthesis of DHEA-S from placental pregnenolone, fetal liver hydroxylation to 16a-OH-DHEAS, followed by placental conversion to estrogens
1. maternal cholesterol -> placenta -> pregnenolone -> fetal adrenal -> DHEAS
2. fetal adrenal DHEAS -> placents -> adrostenedione -> E2 + E
3. fetal adrenal DHEAS -> fetal liver -> 16a-OH-DHEAS -> palcenta -> 16a-OHDEA -> E3
*sulfination of DHEA eliminates any androgenic effects of high DHEA on fetus
(estrogens promote breast development, but inhibit milk production before birth. levels rise constantly through pregnancy. can measure E3 for healthy fetal dev)

50
Q

placental lactogen (PL or hPL)
(or chorionic somatomammotropin, CS)
[placental hormone]

A
  • similar to GH + prolactin (PRL)
  • PL facilitates breast development, maintains pos protein balance, mobilizes fats for energy and promotes high glucose levels required for nourishing fetus (diabetogenic)
  • rises at constant rate through pregnancy
51
Q

parturition (birth)

A
  1. after 30wks, rhythmic uterine contractions inc in strength + duration
  2. after 8mo, uterine shifts toward cervix
  3. after 8.5 mo, dilation + softening of cervix. mediated by E’s, ovarian/placental polypeptide hormone relaxin (insulin/IGF-like) + PGS
  4. efficacy of progesterone in inh contraction dec, probs b/c E is inc synthesized by placenta from fetal adrenal androgens induced by placental CRH-like hormone or ratio and/or distribution of P receptor isoforms change
  5. uterine muscles, now electrically couple via E-ind gap junctions, stimulated by stretch to contract coordinately
  6. oxytocin rec progressively induced by inc E, make uterus inc more sensitive to oxytocin
  7. stim by stretch receptors in uterus/cervix, oxytocin is released from posterior pituitary, inc and synchronizing contractions further (pos feedback) and increasing uterine PG release
  8. sufficient dilation + forcible, rhythmic contractions result in expulsion of fetus + placenta (specific trigger for initiation unclear)
52
Q

estrogen + progesterone: lactation

A
  • E+P (first from corpus luteum, then placenta), PL + PRL, cooperatively stim breast dev, creating components req for milk synthesis, storage, release
  • estrogen stimulates synthesis + sec of prolactin by anterior pituitary
  • but high E+P inhibit milk production until birth. after w/ placenta absence + dec in E+P, can have milk prod (also w/ red prolactin)
  • initial sec is colostrum, more protein and less fat than milk
53
Q

prolactin functions relevant to lactation (3)

A
  1. mammogenesis: growth + dev of mammary gland
  2. lactogenesis: initiation of lactation
  3. galactopoiesis: maintenance of milk production
54
Q

prolactin inh + stim

A
  • prolactin release inh by dopamine (prolactin inhibiting hormone)
  • may be stimulated by a prolactin releasing factor
55
Q

milk ejection (“let-down”) reflex (5)

A
  1. suckling results in neural input to hypothalamus, inh DA release, but stim PRF release
  2. decrease DA allows sec of prolactin, stim milk synthesis in mammary gland
  3. posterior pituitary neurally stim to release oxytocin (suckling)
  4. oxytocin stim myoepithelial cells of breast to contract, ejecting milk
  5. during nursing, neural input + high prolactin in h GnRH release suppressing ovulation (hyperprolactinemia can result in amenorrhea and galactorrhea)

Physio Exam 3 - Endocrine (8 decks)

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