Exam 4: Reproductive Flashcards
Alternate names for mesonephric and paramesonephric ducts:
Meso: Wolffian
Parameso: Mullerian
Development of male fetus:
Y chromosome produces anti-mullerian hormone
Causes paramesonephric duct to shrivel
Preserves mesonephric duct
Development of female fetus:
Anti-wolffian hormone causes mesonephric duct to shrivel
Development of external genitalia is based on:
Androgen levels
Pathway sperm travel through:
Testis Ductus epididymis Ductus (vas) deferens Ampulla Ejaculatory duct Urethra
Glands of the male tract:
Seminal vesicles
Prostate
Bulbourethral (Cowper’s)
Types of cells in the seminferous tubules:
Sertoli
Spermatagonia
Interstitial cells in the testes:
Leydig cells
Reason for fat deposits in the testes:
Need fat for cholesterol for steroids like testosterone!
Effect of exogenous testosterone on the testes:
They will shrink
Role of Sertoli cells:
Support cells that provide growth factors and nutrients for developing sperm cells, influenced by testosterone
Sertoli = FSH Leydig = LH
One spermatogonium becomes:
One daughter spermatogonium
One daughter spermatocyte → 4 sperm
Inhibin and activin are:
Testicular hormones that inhibit/promote FSH secretion in the pituitary
LH effect in the testes:
Stimulates Leydig cells to produce testosterone
FSH effect in the testes:
Stimulates Sertoli cells to Support Sperm production
Testosterone + FSH effect in the testes:
Stimulates Sertoli cells for sperm production
Pathogenesis of benign prostate hyperplasia:
Epithelial cells over-replicate and push on capsule, which compresses the urethra
Prostate cancer basics:
Very slow growing and rarely lethal
Most common metastasis sites are lymph nodes, bones, liver, adrenals
Four zones of the prostate:
Central zone
Peripheral zone
Transitional zone
Periurethral zone
BPH usually starts in the:
Central zone
Prostate carcinoma usually begins in the:
Peripheral zone
Digital rectal exam can feel:
Prostate carcinoma
Bacteria responsible for chlamydia:
Chlamydia trachomatis
Bacteria responsible for gonorrhea:
Neisseria gonorrhoeae
Bacteria responsible for syphilis:
Treponema pallidum
Bacteria responsible for chancroid:
Haemophilus ducreyi
S/s of syphilis:
Painless lesions/ulcerations
Microscopy of syphilis:
Spirochetes on darkfield
HHV strain that causes genital herpes:
HHV-2
S/s of genital herpes:
Painful superficial lesions that begin as vesicles and re-occur in the same place
HHV strain that causes cold sores and the nerve it prefers:
HHV-1; trigeminal
S/s of chancroid:
Wider, deeper, painful ulcers
Genital ulcers, in order of smallest to deepest:
Herpes
Syphilis
Chancroid
Incidence of chlamydia:
10% of women 15-24yo
S/s of chlamydia:
Often asymptomatic
Can cause PID
Scars the fallopian tubes and causes infertility
Strains of HPV that cause warts:
6, 11, etc
Tx of genital warts:
Burning
Freezing
Acid
S/s of gonorrhea:
♂ Yellow/white discharge from penis
♀ Yellow/greenish discharge
Pain/burning during urination
Tx of gonorrhea:
Abx (pcn)
Organism behind trichomonas:
Protozoan; trichomonas vaginalis
S/s of trichomonas:
♂ Asymptomatic
♀ ↑ pH in vagina to 5-6; ↑ in concurrent infections
S/s of scabies:
Itching!! especially in soft, moist, intertriginous regions (groin, axilla, etc)
Crabs are caused by:
Phthirus pubis / pubic louse
Order of follicle development in ovary:
Primordial → primary → secondary → Graafian (mature)
Every month this many primordial follicles start growing:
About a dozen
Stimulus for follicle to burst:
Spike in LH/progesterone and ↑ collagenase
After ovulation, follicle becomes:
Corpus luteum, then corpus albicans (small scar)
Ideally sperm meets egg at:
Ampulla of fallopian tube
Cumulus oophorus is:
Cells surrounding egg that remain around egg after release
Antrum layer is:
Fluid filled layer of follicle, very high in estrogen, that will not let follicle develop
Granulosa layer is:
Closest to the egg; converts androgens to estrogens from the theca interna
Theca internal layer is:
Producer of androgens; LH receptors
Theca externa layer is:
Connective tissue; must be ripped through to ovulate
LH effect in ovaries:
Stimulates the theca interna cells to produce androgens
FSH effect in ovaries:
Stimulates the granulosa cells to convert androgen to estrogen and support egg development
FSH effect in ovaries:
Stimulates the granulosa cells to convert androgen to estrogen and support egg development
Events of preovulatory/follicular/proliferative phase:
Estrogen driven
FSH stimulates follicles and promotes development of endometrium, produces estrogen which stimulates egg
Events of midcycle:
Big surge of LH, FSH, estrogen; follicle ruptures
Events of post-ovulatory/luteal/secretory phase:
LH driven
Follicle becomes corpus luteum and produces progesterone/estrogen
Role of progesterone:
Supports the endometrium until implantation
Estrogen’s effects on pre-ovulatory follicle:
Inihibits normal feedback loop; ↓ FSH and LH, preventing possible development (BCP mechanism)
Estrogen’s effects on mid-cycle follicle:
Positive feedback causes spike of LH/FSH
Hcg produced by:
Newly forming chorion
Hormone tested for to determine pregnancy:
βhCG
Role of HCG in pregnancy:
Looks like LH; binds to corpus luteum to keep it producing progesterone and preserve the endometrium
TSH levels in pregnancy:
↓ because HCG looks just like it
FSH/LH throughout lifespan:
High at birth
Nothing until puberty
Monthly up/down until menopause
Stay up at menopause
HPV causes cancer by:
Blocking tumor suppressor genes and development of cervical intraepithelial neoplasia
High-risk HPV strains:
16, 18, others
Epithelial area at highest risk for cervical cancer:
Squamocolumnar junction; at birth and after the 20s, is tucked up inside cervix and not accessible to HPV; in teens/20s, is more out towards vagina and susceptible
Uterine fibroids also called:
Leiomyomas
Most common female reproductive cancer:
Endometrial cancer
S/s of endometrial cancer:
Bleeding, esp. in post-menopausal women
Salpingitis caused by:
Infection or endometriosis
Pathogenesis of ectopic pregnancy:
Egg gets stuck in tube due to scarring/inflammation
Pathogenesis of PCOS:
FSH and LH get out of sync; LH stimulates androgens but low FSH will leave androgens leftover, unconverted
S/s of PCOS:
Enlarged, cystic ovaries
Facial hair growth
Infertility
Tx for PCOS:
OCPs with 10-14 days progesterone
Metformin
Meds to reduce hair growth (spironolactone)
Meds to achieve pregnancy (Clomid, FSH/LH)
Surgery (ovarian drilling, hair removal)
Ovarian cancer:
High mortality rate/poor prognosis due to no s/s until advanced
Tends to metastasize
Higher risk for BRCA1
90% come from surface epithelial cells
Teratomas typically occur:
Midline or where gonads are
Complete molar pregnancy:
Chorionic villi are all vesicular, no fetal/embryonic tissue (diploid maternal DNA) - positive pregnancy test due to Hcg
Partial molar pregnancy:
Deformed triploid fetus present or diploid paternal DNA
S/s of pre-eclampsia:
Hypertension
Proteinuria
Edema
Pathogenesis of pre-eclampsia:
Hypoalbuminemia; inadequate development of placental spiral arteries, somehow fetus signals to ↑ BP
S/s of eclampsia:
Seizures; can be fatal
Dx’ing amenorrhea:
Progesterone challenge
