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72 Cards in this Set
- Front
- Back
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describe the HPG axis loop
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Hypothalamus produce GnRH
ant pit produces FSH and LH FSH and LH stimulate ovary and testes testicles: testosterone, inhibin ovary: estrogen and progesterone and inhibin the products of ovary and testes feedback to inhibit ant pituitary and hypothalamus |
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what are the two phases of the menstrual cycle
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follicular and luteal
approximately 14 days each luteal phase always 14 days |
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what two phases describe changes in endometrium
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proliferative and secretory
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when does the follicular phase end and beginÉ
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begins with onset of menses ends on day of LH surge
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what hapens to GNRH at the end of the luteal phase and early follicular phase
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withdrawal of E and P releases negative feedback on GnRH
increased GnRH results in 30% increase in FSH |
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what happens in the follicular phase
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FSH release from Ant pituitary results in growth of 5-15 primordial follicles
by late follicular phase a single dominant follicle is selected |
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how is does dominant follicle produce estrogen
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2 step process:
theca interna cells produce androstenedione in response to LH stimulation granulosa cells convert androstenedione to estradiol when stimulated by FSH- |
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what does estrogen do to uterine lining during follicular phase
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causes it to thicken or proliferate
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when does serum estradiol peak
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in follicular phase, approx, 1 day before ovualation
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when does LH spike occur
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day 14 in response to estrogen surge
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what is ovulation
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increase in LH level causes follicle to rupture and release mature ovum
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what makes the LH surge possible
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switch from negative feedback control of LH by E and P to positive feedback
rising estradiol levels lead to 10 fold increase in LH |
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what happens in ovary in response to LH surge
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oocyte in dominant follicle completes first meiotic division
increase in local secretions of plasminogen activator and cytokines required for ovulation oocyte released after 36 hrs of LH surge even before oocyte release, granulosa cells around it begin to leuteinize and produce P P slows LH pulses |
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when does luteal phase begin
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after ovulation and remnants of follicle left behind in ovary develop the corpus luteum
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what happens to egg following ovulation
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ovum passes into fallopian tube and is swept down to uterus by cilia lining the tube
3-4 days to travel down tube to uterus fertilization must occur 24 hours post ovulation or ovum degenerates |
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what forms the corpus luteum
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granulosa and theca interna cells lining wall of follicle form the corpus luteum, stimulated by LH
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what does the corpus luteum synthesize and what does that do the endometrium
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estrogen and large amounts of progesterone
P stimulates endometrium to become more glandular and secretory in preparation for implantation of fertilized ovum |
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if fertlization occurs what is produced, what produces it and what is its function
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trophoblast produces human chorionic gonadotropin, hcg, which maintains corpus luteum so it may continue producing estrogen and progesterone to support endometrium
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what forms 8-10 weeks to take over production of estrogen and progesterone from corpus luteumÉ
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placenta
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what happens in luteal phase if fertilization does not occurÉ
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corpus luteum is not maintained by hcg so it degenerates after 14 days
estrogen and progesterone levels fall causing endometrium to slough off FSH levels rise in absence of negative feedback and MENSTRUATION occurs |
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what is menopause
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defined retroactively 1 year after LMP average age 51
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what is climacteric or perimenopause
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prodrome surrounding the transition to menopause - 45-47 years of age
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what is the pathophysiology of menopause
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the number of primordial follicles shrinks drastically through life cycle until functional
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describe the depletion of primary follicles through life
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newborn 2-3 million
puberty 300,000-400,000 forty years thousands post menopause- few or none |
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what are acute symptoms of menopause
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hot flashes
night sweats insomnia anxietyéirritability memory loss poor concentration mood changes |
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what are intermediate late changes in menopause
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dyspareunia
loss of libido urethral syndrome vaginal atrophy |
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what primary hormone declines in menopause
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estrogen
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what are some multiple sites of estrogen action
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brain
breast heart liver vertebrae genetalia long bones skin |
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what are early clinical px of menopause
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amenorrhea, vasomotor symptoms (hot flashes, nightsweats), and sleep disruption
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what are late clinical px of menopause
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vaginal dryness, dyspareunia
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what are some lab tests in to help define menopause status
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FSH can be transiently elevate in perimenopause
FSH levels are consistently above 30 IUéL are diagnositic of menopause |
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what are some first line health promotion disease prevention methods in post menopausal woman
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exercise, calcium, vitamin d, smoking cessation and moderate alcohol intake
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what are some vasomotor symptoms
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dizziness, headaches, pounding heart, sweating, night sweats, waking
88% of women experience some kind of VMS |
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managing moderate to severe Vasomotor symptoms
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lifestyle changes
HT: estrogen therapy +-progestin SNRI if estrogen not appropriate Gabapentin for toughest |
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what happens to bladder with agingÉ
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urgency frequency recurrent UTI
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what happens to vagina with aging
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dryness, painful intercourse, recurrent infection
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therapy for urogenital atrophy
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lubricants
systemic hormone therapy local vaginal estrogen |
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true or false HT can worsen urinary incontinence
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true, estrogen can improve vaginal epithelial health but can result in decreased periurethral collagen
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tx options for sexual dysfunction
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self education
psychotherapy or marital therapy sexual therapy treat underlying medical condition HT locally or systemic HT and Testosterone |
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estrogen therapy for sexual function increases what?
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frequency of sexual activity
desire arousal enjoyment fantasies satisfaction vaginal lubrication feeling physically attractive |
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estrogen therapy for sexual function decreases what
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dyspareunia
vaginal dryness |
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why does menopause lead to accelerated bone loss
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relative increase in osteoclast activity
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what is the life time risk for any osteoporotic fracture for a 50 year old woman
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40%
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age related relative risk for mortality following a fracture is highest for what type of fractures
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hip and spine
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what are risk factors for fragility fractures
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bone mineral density
previous fractures +family Hx advanced age propensity to falls postural instability nulliparity |
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risks factors for low bone minearl density
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Estrogen deficiency - early menopause, oopherectomy
petite frame genetic physical inactivity poor nutrition cigarette smoking certain meds anticonvulsants, lithium, heparin |
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why do bone densitometry
who to do it on? |
powerful predictor for fragility fractures
assess response to tx who estrogen deficiency now or previously those uncertain about HRT those who had prior fracture anyone over 65 |
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fracture risks for
osteopenia osteoporosis severe osteoporosis |
2 fold
4-5 fold 20 fold |
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is HT effective at low doses for preservation of spinal BMD
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yes
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what happens to BMD after HRT stopped
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lost rapidly
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what role does HT play in post menopausal bone loss and fractures
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prevents PM bone loss
reduces both vertebral and non-vertebral fractures and the loss of teeth |
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what were the major criticisms of WHI study
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dramatic media release
over extrapolation: study had more older women, used that data for recommendations to younger women lots of biases |
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Does HT have benefit for cardiovascular health
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yes for younger postmenopausal women
more adverse effects when started in older women few CV risks and more benefits when started in younger menopausal women |
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what is the impact of HT on cognition in postmenopausal women
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little evidence of any affect
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estrogens role in depression
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can be used in tx of ppD
can improve mood in post menopausal women without clinical depression can improve depressive nature in perimenopausal women |
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WHat is the role of hormone use in BC?
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E+P use greater than 5 years associated with increased risk of BC
the risk disappears 5 years after stopping HT increased risk for E+P combo than just E |
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what can be given to reduce hyperplasia and malignancy in endometrial cancer
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progestin- cyclic or continous
uterus present: E +P or E alone uterus absent E |
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name 2 tests to monitor endometrial health
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endometrial biopsy
transvaginal USS of endometrial thickness |
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Indications for peri and post menopausal HT
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vasomotor symptoms
urogenital atrophy symptoms prevention and tx of osteoporosis |
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what are some contraindications for HT use
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acute liver disease
concurrent breast cancer undiagnosed breast lump unexplained uterine bleeding active thromboembolic disease certain thrombophilias prior VTE |
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what are options for delivering Estrogen
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tablets- oral, vaginal
skin patches topical gels injections vaginal creams and ring |
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options for delivering progestin
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tablets
skin patches |
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where does spermatogenesis occur
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seminiferous tubules of testis
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describe process of spermatogenesis
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germinal epithelium gives rise to spermatogonia (2n)
spermatogonia gives rise to A and B cells, via mitosis A replenishes stock, B gives rise to spermatocytes spermatogonia increase in size and number to form primary spermatocytes primary spermatocytes undergo meiosis 1 to become secondary spermatocytes secndary spermatocytes undergo meiosis 2 to become 4 haploid spermatids |
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describe changes in spermatids as they mature
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spermatids undergo spermiogenesis: changes shape, elongates, develops acrosomes,
nucleus enlarges and etrudes into sertoli cells |
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what forms the flagella of the spermatozoa and why is it used
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centriole- for propulsion
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why do mitochondria congregate in the neck of sperm
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atp for movement
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what process must the mature sperm undergo to fertilize an oocyte?
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capacitation
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how long is the spermatogenesis process
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64 days
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describe beginning of Oogeneis
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7th week in gestation
secondary germinal cords decompose into groups of cells priliferation ensues- |
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at what week does oogonia commence meiosis and become primary oocytes
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12 weeks
they arrest in first meiosis can last till adulthood |
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what does primary oocytes become covered by?
what is it called now |
granulosa cells
primordial follicle |
