Test 1 Flashcards
FSH in males
- acts on seminiferous tubules to produce sperm
- acts on seminiferous tubules to release inhibin B
inhibin B
acts on anterior pituitary to inhibit production of FSH
LH in males
- acts on Leydig cells to produce testosterone
- testosterone has negative feedback on anterior pituitary to inhibit LH
hypogonadotropic hypogonadism pathophysiology
- secondary
- pituitary does not secrete enough LH and FSH
hypogonadotropic hypogonadism causes
- hyperprolactinemia (increased dopamine inhibits GnRH)
- Kallmann’s syndrome
- opiates
- diabetes
- GnRH agonist therapy (prostate cancer)
hypogonadotropic hypogonadism labs
- low or normal LH
- low FSH
- low testosterone
Kallmann’s Syndrome characteristics
- X linked recessive trait
- most common congenital gonadotropin deficiency
- micropenis and cryptorchidism
- cleft lip
- hearing loss
- abnormal tooth
- can’t distinguish odors
hypergonadotropic hypogonadism
- primary gonadal dysfunction
- failure in testosterone = increased LH
- sertoli cell dysfunction = increased FSH
hypergonadotropic hypogonadism labs
- low testosterone
- increased LH
- increased FSH
- usually low sperm count
Klinefelter’s Syndrome
- hypergonadotropic hypogonadism
- XXY (diagnose with chromosome analysis)
- infertile or reduced fertility
Klinefelter’s Syndrome physical characteristics
- breast development
- small testicular size
- female pubic hair pattern
- tall, thin, long arms
- azoospermia
cryptorchidism
- one or both testes fail to descend from abdomen
- most common defect of male genitals
- most descend within first year
cryptorchidism treatment
- orchioplexy
- untreated has higher risk of testicular cancer
anorchia
- both testes absent at birth
- fail to develop within 8 weeks = female genitalia develop
- develop but lose function 8-10 weeks = ambiguous genitalia
- function loss after 14 weeks = partial male genital with no testes
HCG stimulation/challenge
- collect basal and post HCG injection testosterone
- Increase = cryptorchidism
- Absence = anorchia
HCG causes leydig cells to secrete androgens
natural decline in testosterone
- decreased libido
- fatigue
- elevated LH
- low testosterone
- low sperm
defects in androgen action physiology
- testosterone normally binds to androgen receptors
- absence of receptors cause testicular feminization
defects in androgen action labs
- elevated testosterone
- elevated LH
defects in androgen action labs
- intersex
- 5 alpha reductase enzyme deficiency
intersex physiology
- born with primary sex characteristics of one sex
- develop secondary sex characteristics different than expected
- cryptorchid
androgen insensitivity
- partial resistance to testosterone
- hypogonadism
- cryptorchidism
- gynecomastia
- serum testosterone is normal
testosterone labs
- evaluate in morning with highest level at 0800
- excess production induces premature puberty in males
- assess hypogonadism, pituitary gonadotropin, impotency, cryptorchidism, and part of infertility
FSH in females
- stimulates development of follicles in ovaries
- acts on granulosa cells
LH in females
- stimulates development of corpus luteum in ovaries
- acts on theca interna cells
- surge causes ovulation
how is number of days in menstrual cycle determined
time required for development of follicles and corpus luteum after menstruation and feedback effect of estrogen and progesterone
estrogen
- estradiol, estrone, and estriol
- made by ovary
estrogen stimulate growth and development of
- uterus, fallopian tubes, vagina, external female sex organs
- endometrial proliferation
- breast development
- skeletal growth
- fat deposition
progesterone
- produced by corpus luteum
- best test to determine if ovulation has occurred
menses steps
- pituitary secretes LH and FSH
- estrogen inhibits secretion of LH and FSH
- pituitary secretes large amount of LH (despite inhibition) immediately before ovulation
- after ovulation corpus luteum secretes estrogen and progesterone to inhibit LH and FSH
- degradation of corpus luteum causes estrogen and progesterone levels to fall, allowing LH and FSH levels to rise
primary amenorrhea
-no menses by age 16
or
-no menses by 14, absence of breast development, and less than 3% height for age range
primary amenorrhea pearls
- if normal pubertal development think structural
- if delayed pubertal development thing genetic
turner syndrome
- primary amenorrhea cause (premature ovarian failure)
- most common chromosomal abnormality, XO
- short stature with webbing of neck
turner syndrome labs
- high LH
- high FSH
turner syndrome treatment
- growth hormone
- age <12 androgen therapy
- age >12 hormone replacement with estrogen/progesterone
secondary amenorrhea
-had menses but no menses for 3-6 months
causes of secondary amenorrhea
- pregnancy most common
- menopause second most common
- premature ovarian failure
menopause
- high FSH
- no menses for 12 months
premature ovarian failure
- menopause under the age of 40
- FSH and LH are elevated
secondary amenorrhea caused by hypothalamic pituitary issues
- low frequency of GnRH pulses
- hyperprolactinemia
- Low to normal FSH
- high prolactin
PCOS pathophysiology
- rapid GnRH pulses increase LH synthesis with excessive androgen secretion
- excess androgens cause hirsutism, development of male characteristics, and amenorrhea
- infertility varies
PCOS physical presentation
- history irregular menses
- androgenic features
- central obesity
- mood disturbance
PCOS labs
- insulin resistance
- LH exaggerated surge
- testosterone >20
- dyslipidemia
- pelvic ultrasound not required for diagnosis
asherman syndrome
- caused by infection of uterine lining (endometriosis) or vigorous curettage causing scarring
- causes secondary amenorrhea with normal FSH
- estrogen and progesterone given after scar tissue removed
- high risk for spontaneous abortion
progesterone withdraw test
- administer progesterone for 10 days
- therapeutic and diagnostic
- withdraw of medication should cause bleeding
- absence of bleeding indicates lack of estrogen or uterine abnormality