• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/78

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

78 Cards in this Set

  • Front
  • Back
excessive terminal hair growth in locations where hair growth is normally minimal or absent
hirsutism
in the absence of gonadal androgen production, hair growth does not proceed which Tanner stage
Tanner stage 2
*gonadal androgens are reponsible for normal progression from Tanner 3-5
what does androgen stimulation do to terminal hair in scalp
recede and turn to fine vellus hair
what two enzymes do hair follicles contain and what do they form
17-ketosteroid reductase (androstenedione --> testosterone)
5a-reductase (testosterone --> DHT)
what two androgens stimulate hair growth, pigmentation, and sebum production
testosterone
dihydrotestosterone
what hirsute women have increased activity in what enzyme
5a-reductase
*with normal serum androgen levels
what two hormones control androgen production in adrenals vs. ovaries
adrenal production - controlled by ACTH
ovarian production - controlled by LH
3 androgens produced in women and their site of synthesis
1. androstenedione - 50/50 andrenal and ovary
2. DHEA and DHEA-S - adrenal glands
3. testosterone - 25% ovaries and 75% extraglandular tissue from circulating androstenedione and DHEA
characteristics of virilization
frontal balding
seborrhea
acne
clitoromegaly
what is the amount of virilization directly proportional to
amount of androgen production
most common cause for pathologic hirsutism and androgen excess in women
polycystic ovarian syndrome
clinical presentation of polycysitc ovarian syndrome
obesity
hirsutism
secondary amenorrhea
insulin resistance
mechanism for increased androgen and estrogen in polycystic ovarian syndrome
1. increased GnRH and LH favor production of androstenedione by ovarian theca cells
2. excess androstenedione is converted to testosterone by 17-ketosteroid reductase in theca cells and aromatized to estrone by ovarian granulsa cells
3. estrone is converted to estradiol by 17B-hydroxysteroid dehydrogenase in skin, adipose tissue, and breast tissue
what hormones are in excess in polycystic ovarian syndrome
androstenedione
testosterone
estrone
estradiol
what is the LH/FSH ratio seen in polycystic ovarian syndrome
LH/FSH > 2.5
what does insulin resistance in polycystic ovarian syndrome lead to
1. acts synergistically with LH to increase testosterone production by theca cells
2. decreases hepatic synthesis of sex-hormone binding globulin to increase free testosterone levels
what do excess insulin and estrone lead to in polycystic ovarian syndrome
excess estrone and insulin - stimulate LH secretion
excess estrone - inhibits FSH secretion
what causes the chronic anovulation in PCOS
excess LH and deficient FSH
the risk of developing what cancer is increased in PCOS
endometrial carcinoma due to increased estradiol
what is the most sensitive lab measure of androgen excess in PCOS
increased plasma free testosterone
anti-estrogen drug that increases secretion of FSH and LH
clomiphene
differentiate developing of hirsutism in women with androgen-secreting tumors vs. PCOS
androgen tumors - rapid development in their 3rd decade
PCOS - slow onset
differentiate androgen-secreting tumors in the ovary vs. adrenal gland
ovary - markedly increased serum testosterone, no increase in DHEA or DHEA-S
adrenal - markedly increase levels of DHEA and DHEA-S, but slightly elevated testosterone
which congenital adrenal hyperplasia is associated with hypertension
11B-hydroxylase deficiency due to excess DOC (deoxycorticosterone)
hormone levels associated with 21a-hydroxylase deficiency
decreased cortisol
increased ACTH
increased DHEA and DHEA-S
what happens when patient with 21a-hydroxylase deficiency is given exogenous administration of ACTH
causes marked elevations of 17a-hydroxyprogesterone
*diagnostic
what can prolactin stimulate production of
DHEA-S
medications associated with hirsutism
minoxidil
cyclosporine
phenytoin
what is the general cause of primary amenorrhea
chronically low levels of estrogen
3 categories of primary amenorrhea
1. hypergonatotropic hypogonadism
2. hypergonatotrpic hypogonadism
3. structural abnormalities
4 causes for hypogonadotropic hypogonadism
1. Turner's syndrome
2. pure gonadal dysgenesis
3. 17a-hydroxylase deficiency
4. resistant ovary syndrome
what does an arm span greater than body height signify
hypogonadism because decreased estrogen is unable to close epiphyseal plates
FSH, LH, and estrogen levels of person with Turner's
elevated FSH and LH
decreased estrogen
two disorders associated with streak ovaries
1. Turner's
2. pure gonadal dysgenesis
two disorders associated with being tall in stature due to decreased estrogen
pure gonadal dysgenesis
17a-hydroxylase deficiency
FSH, LH, and estrogen levels in all hypergonadotropic hypogonadism disorders
elevated FSH and LH
decreased estrogen
this disorder lacks normal FSH receptors
resistant ovary syndrome
two disorders with hypogonadotropic hypogonadism
1. insufficient body fat to trigger menarche
2. Kallmann syndrome
this syndrome is associated with decreased FSH, LH, estrogen with anosmia
Kallmann syndrome
3 structural abnormalities associated with primary amenorrhea
1. genital outflow obstruction (imperforate hymen or labial fusion)
2. Mullerian agenesis
3. androgen insenstivity syndrome
primary amenorrhea disorders with normal FSH, LH, and estrogen
genital outflow tract obstruction
mullerian agnesis
this patient with primary amenorrhea presents with elevated LH and serum testosterone with sparse pubic and axillary hair growth
androgen insensitivity syndrome
absence of menstruation for a period of three months in a woman who has previously menstruated
secondary amenorrhea
causes of secondary amenorrhea (7)
1. menopause
2. pregnancy
3. hypothalamic chronic anovulation
4. hyperprolactinemia
5. PCOS
6. premature ovarian failure
7. Asherman's syndrome
what causes secondary amenorrhea in female athlete's triad
disturbance in pulsatile GnRH release by the hypothalamus
Female athlete's triad
disordered eating
amenorrhea
osteoporosis
cause of secondary amenorrhea in prolactinoma
elevated prolactin interferes with cyclic release of GnRH
this disorder is associated with acanthosis nigricans
PCOS
this only secondary amenorrhea with elevated LH, androgens, and estrone
PCOS
genetic cause for secondary amenorrhea
premature ovarian failure: deletions or structural abnormalities in the X chromosome, need two intact X chromosomes for maintenance of oocytes
FSH and LH levels seen in premature ovarian failure
elevated due to loss of negative feedback from sex hormones
acquired secondary amenorrhea
Asherman's syndrome due to uterine infections or scarring
secondary amenorrhea associated with normal FSH, LH, and estrogen
Asherman's syndrome
first test in patient presenting with amenorrhea
B-hCG
patient presents with amenorrhea, medroxyprogesterone was administered and bleeding began a few days later after drug was stopped
PCOS
what should be measured if no bleeding occurs after medroxyprogesterone therapy
FSH and LH
elevated FSH - premature ovarian failure
normal/low - hypothalamic/pituitary disorder or anatomic abnormality
differentiate if a patient bleeds after administration of OCP after medroxyprogesterone test
bleed - chronic anovulation with low estrogen
no bleed - outflow tract obstruction or Asherman's syndrome
what causes chronic anovulation with excess estrogen
PCOS
the only congenital adrenal hyperplasia with elevated FSH and LH and sexual infantilism
17a-hydroxylase deficiency
what three hormone levels should be tested in a patient presenting with secondary amenorrhea
B-hCG
prolactin
TSH
period of irregular menstrual cycles in the premenopausal period
climacteric
elevated gonadotropin in climacteric period
FSH
FSH, LH, estrogen, and testosterone levels in menopause
elevated FSH, LH, and testosterone
decreased estrogen
predominant estrogen in postmenopausal woman
estrone
androgen/estrogen ratio in menopause
increased due to large reduction in estrogen synthesis and mild reduction in androgen synthesis
where is nearly all the estorgen derived from in menopause
aromatization of adrenal androstenedione
what causes hot flashes
CNS norepinephrine increase rests hypothalamic thermostat upward and causes reflex sweating and cutaneous vasodilation
cholesterol levels in menopause
total and LDL cholesterol increase
HDL cholesterol decrease
what directly causes osteoporosis in menopause
hypoestrogenism
*estrogen helps converse Ca in both the GI and kidney, Ca wasting occurs and PTH rises secondarily
what do osteoblasts secrete to inhibit binding of RANKL
osteoprotegerin
what does estrogen deficiency do to production of RANKL and osteoprotegerin
increase in RANKL production
decrease in OPG production
receptor activation of nuclear factor kB on the osteoclast membrane
RANK
what are the three categories of germ cell tumors and associated with tumors
no differentiation - dysgerminoma
embryonic tissue - teratoma
extraembryonic tissue - endodermal sinus or choriocarcinoma
which germ cell tumor is associated with lymphocytes present in fibrous stroma of the tumor
dysgerminoma
these tumors are associated with secreting high levels of chorionic gonadotropin (hCG)
choriocarcinoma
what do choriocarinomas and hydatidiform moles have in common
both secrete high levels of B-hCG
what ovarian tumor is associated with secreting a-FP
endodermal sinus tumor
which hydatidiform mole is associated with progression to choriocarcinoma
complete hydatidiform mole