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44 Cards in this Set
- Front
- Back
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events of puberty
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increase fat - increaaseleptin - increasae GnRH pulses
increase LH & FSH pulses ovarian folliclesdevelop - increaseandrogens (testosterone & androstenedione) and increase female hormones (estradiol) released secondary sexual characteristics: pubarche graafianfollicle - ovulation - corpus luteum menarche : onset of menses |
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consequencesof puberty
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breastdevelopment
further changes in uterus, vagina with improved fertility growth spurtthen epiphyseal closure effectsof estradiol on other parts of thebody - brain - immune system - lipids & CV system |
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requirements for normal ovulatory menstrual cycles
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hypothalamus
pituitary ovary uterus & patent vagina no other illness, fever, stress, or wt fluctuations |
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regulation of GnRH ,LH & FSH secretion
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locally synthesized and systemic hormones regulatethe pulsatilesecretion of GnRH frmthe hypothalamus into the portal circulation
GnRH together with number of steroid & peptidehormones regulate the syn of a and b gonadotropin subunits & formation and secretion of FSH and LH |
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normal monthly menstrual cycle
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menses
- FSH rise - estradiol rise - basal body temp low - endomtrial develoment low proliferative phase - FSH decrease, then peaks at end - LH on the rise - estradiolpeaks at end - progesterone low - body temp low - some follicular development and ovulation at end - endometrial development increases secretory phase - FSH decreases - LH slightly increase - progesterone increases and then decreases - increase in basal body temp by 0.5 C - corpus luteum after ovulation - high endometrial development |
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menses does not equal ovulation
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mensescan occur without ovulation: estrogen from fat can stimulate endometrial prolif
ovulation can occur without menses: no endometrium amenorrhea: - primary vs secondary hypogonadism: cause - primary vs secondary amenorrhea: timing irregular menses (oliomenorrhea): intermittent or no ovulation |
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how do you knowif cycles are ovulatory
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progesterone/luteal phase indicators
- change in basal body temp mid cycle - luteal progesterone (day 21-25) elevatted - luteal phaseendometrail biopsy shows secretory changes -premenstrual symptoms LH peak at ovulation; at home kits |
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how does female hypogonadism present
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pre natal:
- subtle: normal femaleexternal genitalia, may be unrecognized unil puberty when no sexual maturation unless other stigmata - turner's peri puberty - no sexual maturation - no menarche: no primary amenorrhea post puberty - loss of menses : secondary amenorrhea - wrinkles - vaginaldryness: painfulintercourse ; dyspareunia - hot flashes if LH/FSH high |
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pertinent history for hypogonadism
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was sexual development normal?
- age of secondary sexual characteristics or menses; regular or not? history of hyperandrogenism: excessive hair or acne? history of infertility or preg? history of galactorrhea: suggesting hyperprolactinemi? any other disease/conditions? - stress: depression, eating disorders, sudden severewtchange, fever,elite exercise (ballet) - meds, drug abuse - head trauma or radiation - thyroid or other systemic disease |
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PE of hypogonadism
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insulin resistance phenotype: HTN,ab obesity, acnthosis, acne
hair pattern: distribution, excessive or scant breast exam: normal development, galactorrhea pelvic exam: ovarian mass, gravid uterus other: thyroid, other systemic disease |
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labs for hypogonadism
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estradiol
LH FSH prolactin thyroid tests: free T4 & TSH preg test additional testing if indicated: androgens (freeand total T, DHEA-S), 17-OH-progesterone |
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primary hypogonadism
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ovarian failure
high LH & FSH |
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secondary hypogonadism
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pituitary or hypothalmic
LH & FSH inappropriately normal |
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primary amenorrhea
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neverhad ovulatory cycles
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secondary amenorrhea
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ovulation then stopped
primary and secondary amenorrhea can both be caused by primary or secondary hypogonadism |
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forprimary amenorrhea, consider
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genetic, development causes
hypothalamic/pit: anorexia, illness, prolactin, hypopituitarism, craniopharyngioma ovarian: turner's structural: absent uterus, imperforate vagina other: hormoneaction (androgen insensitivity), preg, thyroid, PCOS, other hyperandrogen states |
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Turner's syndrome common features
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lymphedema
webbed neck high arched palate short 4th metacrapal shield chest increased carrying angle strabismus ptosis multiple pigmented nevi |
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Turner's structural anomalies
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coarctation or other CV anomalies in 55%
renal anomaliesin 39% ; horseshoe kidney other: hypothyroidism & diabetes |
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Turner's evaluation
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suspect with px findings
- short stature & slowed growth +/- webbed neck - no or little sexual development - usually primary but may have secondary amenorrhea lab confirmation: LH & FSH increased ; after age of puberty - genotype : XO |
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Turner's tx
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GH for growth
sex steroid replacementafter reaching growth goals |
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case of primary amenorrhea
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testicular feminization syndrome : XY
estradiol "normal" LH, FSH & T increased remove tests: begin sex steroid replacement therapy |
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primary amenorrhea summary
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definition: no prior menses
causes - high LH & FSH: primary - normal LH & FSH: secondary congenital and developmental disorders more likely |
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acquired disorders of secondary amenorrhea
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hypothalamic/pit: anorexi, illness, prolactin,other pit tumors, infarction
ovarian: premature failure: radiation, chemo,surgical, immunologic; menopause structural: hysterectomy,asherman's syndrome other: preg, thyroid PCOS,other hyperandrogen states, systemic illness |
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16 yo girl present for eval of secondary amenorrhea; menarche was at age 12; since started running, her periodshave become lighter andless frequent; LMP 6 months ao; haslost 5 lb over 3 months; runs 6 mi/day, 5x /wk; BMI 19
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functional hypothalamic amenorrhea
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30 yo woman with history of no menses since stopped taking oral contraceptives 6 months ago ; puberty was normal; BMI 21; no galactorrhea, hirsutism, or acne; pevlic exsm normal, preg test neg; prolactin level normal and FSH in menopausal range
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premature ovarian failure
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PCOS
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phenotype, not disease
affects 5-10% of adolescent & adult women characteristic presentation multiple causes no single identifying test: dx of exclusion typically induced by obesity |
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characteristic presentation of PCOS
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anovulatory cycles: amenorrhea,oligomenorrhea
hyperandrogenism: hirsutism, acne, frontal balding +/- infertility |
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Hirsutism
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increase in androgen depednet terminal hair
lip chin chest ab back hypertrichosis: excessive androgen independent hair: non sexual areas ferriman gallwey scoring system normal : 7 |
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recognizing insulin resistance
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ab obesity
acanthosis nigricans: dirty neck hyperandrogenism: hirsutism high TG low HDL pre diabetes H/O gestational diabetes, +FH type 2 dm amenorrhea correlates with wt gain do not need pelvic US |
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tx of PCOS due to insulin resistance depends on pt goals
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hyperandrogenism or irregular/heavy menses
- improve insulin resistance: wt loss, exercise, insulin sensitizing agents - reduce androgens: birth control pill (increases SHBG that binds T and decreases Free T and helps with hirsutism & acne), spironolactone (blocks action) - hair specific aproaches: shaving, bleaching, electrolysis, laser, vaniqa: ornithin decarboxylase inhibitor imrpove fertility: wt loss, metformin, stimulated cycles : clomiphene |
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secondary amenorrhea summary
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definition: loss of menses, when previously normal
distinguish causes - LH & FSH high: primary (menopause) - LH & FSH "normal" : secondary (PRL,stress; needs MRI) - LH/FSH high: consider PCOS |
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HRT
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not one therapy
- many estrogens (potency) and vehicles (patch, pill, shot, vaginal) - many types: androgenic effect - many vehicles: patch or pill ;creams not absorbed - pattern: continuous or cyclic if uterus present, always use progesterone to avoid endometrial hyperplasia & cancer age affects therapy: risk, type, duration |
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indications for HRT
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achieve & maintain peak bone mass in young woman : age < 50 y
symptoms: perimenopause: hot flashes, vaginal irriation, sleep disturbance dissease prevention? risks vs benefits |
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contraindications for estrogen
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H/O deep venous thrombosis or pulmonary emolism, particularly if on E at the time
H/O E responsive cancer: breast & uterine severe untreated TG > 1000 mg/dl |
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benefits of HRT
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build, maintain bones & prevent fracutres
- mortalty of hip fracture > endometrial cancer symptoms of menopause: hot flashes, vaginal itching, painful intercourse, urinary tract infections, urinary incontinence, fuzzy thinking, depression prevents diabetes or colon cancer in some studies |
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risks of HRT in women > 50
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no change in overall mortality
DVT increases 200% ; less with aspirin or statins - all ages - for both E+P & E alone - increase most with age, BMI, LE fracture, recent hospitalization or surgery, leiden factor V (7x risk) - more with oral than transdermal? uncertain stroke CHD breast cancer gallbladder disease |
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women > 50 risk for stroke with HRT
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for both E + P and E alone
all age groups independent of other riskfactors for stroke |
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women > 50 risk for CHD with HRT
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only risk if
- E + P ; not E alone - age dependent: risk only for women > 10 yr after menopause (60 yr +) |
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women > 50 risk for breast cancer & gallbladder disease
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breast cancer increase 20% after 5-10 yrs
- not observed with long term BCP n young women - ONLY E + P ; not E alone - occurs with all E, cyclic/continous, oral or transdermal gallbladder disease - for E and E+P |
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benefits < 50 yo for HRT
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improve symptoms
attain or maintain bone prevent CV progression risks: - DVT : minimal in most - breast Ca, MI, GB dz NOT increased |
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benefits & risks for HRT > 50 yo
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benefits
- decrease symptoms, fractures, new onset diabetes & colorectal cancer (E+P only for colorectal cancer) risks: - DVT: reducedby ASA, statins - breast cancer: E+P only - nonfatal MI : E+P only -nonfatal stroke >65 |
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HRT and menopause management
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<50 : consider HRT until ae 50 if no contraindiation
>50: use for symptoms - <5 y little risk if no specific contraindications - 5-10 yrs: mininmal risk: individual decision - >10 yrs: increasing risk for DVT, stroke& breast cancer all womenneed mammography & DXA for bone density |
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alternatives to HRT for managementof hot flashes
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exercise, soy, neurontin, SSRI, P, clonidine, androgens
dont' work: dong quai, evening primrose oil, vitamine E. black cohosh, or acupuncture Selectiveestrogen R modulators: SERMS; tamoxifen, raloxifene - increase hot flashes |
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alternatives to HRT for management of osteoporosis & CVD
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osteoporosis: bisphosphonates, Ca, Vit D
- 25 OH vit D levelshould be >30 mg/ml CVD: treat risk factors; ASA |
